Intelligent Design Creationists are still trying to promote their views. They consistently claim to have positive evidence of intelligent design and they consistently complain whenever we point out what they actually do; they attack evolution/science. Their main talking point relies on the fallacy known as "false dichotomy." They assume that by casting doubt on evolution/science they lend support to their religious viewpoint.Each year, the IDiots on Evolution News & Views (sic) publish their top ten stories. The series is linked to a fund-raising campaign so it's safe to assume they think these stories advance their cause. Let's see how many of the top stories promote intelligent design and how many are just criticisms of evolution/science. That should be revealing ...
Saturday, December 31, 2016
Tuesday, December 20, 2016
The frequency of blood type O is very high in some populations of native Americans. In many North American tribes, for example, the frequency is over 90% and often approaches 100%. A majority of individuals in those populations have blood type O (homozygous for the O allele). [see Theme: ABO Blood Types]Since there's no solid evidence that blood types are adaptive,1 the standard explanation is random genetic drift.
Jerry Coyne explains it in Why Evolution Is True.
One example of evolution by drift may be the unusual frequencies of blood types (as in the ABO system) in the Old Order Amish and Dunker religious communities in America. These are small, isolated, religious groups whose members intermarry—just the right circumstances for rapid evolution by genetic drift.
Accidents of sampling can also happen when a population is founded by just a few immigrants, as occurs when individuals colonize an island or a new area. The almost complete absence of genes producing the B blood type in Native American populations, for example, may reflect the loss of this gene in a small population of humans that colonized North America from Asia around twelve thousand years ago.
Thursday, December 15, 2016
The lead editorial in last week's issue of Nature (Dec. 8, 2016) urges us to Take the time and effort to correct misinformation. The author (Phil Williamson) is a scientist whose major research interest is climate change and the issue he's addressing is climate change denial. That's a clear example of misinformation but there are other, more subtle, examples that also need attention. I like what he says in the opening paragraphs,
Most researchers who have tried to engage online with ill-informed journalists or pseudoscientists will be familiar with Brandolini’s law (also known as the Bullshit Asymmetry Principle): the amount of energy needed to refute bullshit is an order of magnitude bigger than that needed to produce it. Is it really worth taking the time and effort to challenge, correct and clarify articles that claim to be about science but in most cases seem to represent a political ideology?I've had a bit of experience trying to engage journalists who appear to be ill-informed. I've had little success in convincing them that their reporting leaves a lot to be desired.
I think it is. Challenging falsehoods and misrepresentation may not seem to have any immediate effect, but someone, somewhere, will hear or read our response. The target is not the peddler of nonsense, but those readers who have an open mind on scientific problems. A lie may be able to travel around the world before the truth has its shoes on, but an unchallenged untruth will never stop.
I agree with Phil Williamson that challenging falsehoods and misrepresentation is absolutely necessary even if it has no immediate effect. Recently I posted a piece on the misrepresentations of the ENCODE results in 2007 and pointed a finger at Nature and their editors [The ENCODE publicity campaign of 2007]. They are responsible because they did not ensure that the main paper (Birney et al., 2007) was subjected to appropriate peer review. They are responsible because they promoted misrepresentations in their News article and they are responsible because they published a rather silly News & Views article that did little to correct the misrepresentations.
That was nine years ago. Nature never admitted they were partly to blame for misrepresenting the function of the human genome.
Wednesday, December 14, 2016
ENCODE1 published the results of a pilot project in 2007 (Birney et al., 2007). They looked at 1% (30Mb) of the genome with a view to establishing their techniques and dealing with large amounts of data from many different groups. The goal was to "provide a more biologically informative representation of the human genome by using high-throughput methods to identify and catalogue the functional elements encoded."The most striking result of this preliminary study was the confirmation of pervasive transcription. Here's what the ENCODE Consortium leaders said in the abstract,
Together, our results advance the collective knowledge about human genome function in several major areas. First, our studies provide convincing evidence that the genome is pervasively transcribed, such that the majority of its bases can be found in primary transcripts, including non-protein-coding transcripts, and those that extensively overlap with one another.ENCODE concluded that 93% of the genome is transcribed in one tissue or another. There are two possible explanations that account for pervasive transcription.
Tuesday, December 13, 2016
A reader pointed me to the ThermoFisher Scientific website. ThermoFisher Scientific is a major supply of scientific equipment and supplies. They created their life sciences wesite to help inform their customers and sell more products. The page I'm interested in is: Overview of Post-Translational Modifications (PTMs). It begins with,
Within the last few decades, scientists have discovered that the human proteome is vastly more complex than the human genome. While it is estimated that the human genome comprises between 20,000 and 25,000 genes (1), the total number of proteins in the human proteome is estimated at over 1 million (2). These estimations demonstrate that single genes encode multiple proteins. Genomic recombination, transcription initiation at alternative promoters, differential transcription termination, and alternative splicing of the transcript are mechanisms that generate different mRNA transcripts from a single gene (3).
The increase in complexity from the level of the genome to the proteome is further facilitated by protein post-translational modifications (PTMs). PTMs are chemical modifications that play a key role in functional proteomics, because they regulate activity, localization and interaction with other cellular molecules such as proteins, nucleic acids, lipids, and cofactors.
Saturday, December 10, 2016
It's been twenty years since Michael Behe published Darwin's Black Box and Intelligent Design Creationists are flagellating themselves over the fact that it had so little impact on creationism. The USA is becoming more secular with each passing year. Religion is on the decline.In their attempt to deal with their defeat, the main ID blog has been publishing "Behe's Greatest Hits," which is a euphemistic way of saying "Behe's Greatest Failures." The latest one caught my eye. It's Best of Behe: An Open Letter to Professors Kenneth Miller and PZ Myers.
It takes you back more than two years to July 21, 2014. That's when Michael Behe issued his challenge to PZ Myers and Ken Miller. The challenge was based on his book The Edge of Evolution and specifically on the development of chloroquine resistance in Plasmodium falciparum. Behe starts with the assumption that cloroquine resistance is extremely rare—it occurs with a probability of roughly 10-20. He concludes that resistance requires at least two different mutations that must occur simultaneously in an individual suffering from malaria while being treated with chloroquine.
The first assumption is approximately correct. Chloroquine resistance is rare. He was criticized for the second assumption; namely, that the overall probability of chloroquine resistance is just the probability of two mutations occurring simultaneously (e.g. 10-10 × 10-10 = 10-20).
The International Humanist and Ethical Union (IHEU) is a collection of Humanist, atheist, secular and similar organizations from many countries. It publishes the Freedom of Thought Report, which purports to be, "A global report on discrimination against humanists, atheists, and the nonreligious." The group intends to highlight systemic discrimination.
We believe it is important to document discriminatory national laws and state authorities which violate freedom of religion or belief and freedom of expression. As well as affecting the overtly nonreligious, such as atheists and Humanists, such systemic discrimination also often affects the religious, in particular minorities and non-conformists, and the unaffiliated (those who hold no particular religion or worldview-level belief).There are four categories of systemic discrimination: Constitution and government; Education and children’s rights; Family, community, society, religious courts and tribunals; and Freedom of expression advocacy of humanist values. For each category there are six possible rankings [see Ratings System]:
Systemic, legal discrimination can include such things as established state churches (resulting in religious privilege), religious instruction provided without secular ethical alternative classes in schools, through to severe punishments such as prison for crimes of “insulting” religion, or death merely for expressing your atheism.
Here's the result for the entire world.Black = Grave Violations
Red = Severe Discrimination
Orange = Systemic Discrimination
Yellow = Mostly Satisfactory
Green = Free and Equal
Gray = No Rating
Canada is ranked as "Systemic Discrimination" in all four categories. The USA gets the best rating (Free and Equal) in two categories: "Education and children’s rights" and "Freedom of expression advocacy of humanist values." It gets the second highest rating (Mostly Satisfactory) in: "Constitution and government" and "Family, community, society, religious courts and tribunals."
The conclusion is obvious. If you are an atheist you are much better off living in the USA than in Canada!
Hemant Mehta, better known as The Friendly Atheist, published the same figure on his blog a few days ago [New Report Highlights the Worst Countries in the World for Atheist Citizens. Many Canadians responded in the comments. One of them, CanuckAmuck, said,
I am dubious about some of the standards of this report. Not to appear butthurt, but to equate Canada to Russia in terms of "Constitution and the Government" is to say the least, asinine. And to report that "Society and Community" is "graver" for the atheist here than in the U.S. is likewise so.I agree completely. Read the other comments to see what others think of this report.
Respond in the comments if you think atheists are better off in the USA than in Canada.
Friday, December 09, 2016
We've been having a discussion about function and how to recognize it. This is important when it comes to determining how much junk is in our genome [see Restarting the function wars (The Function Wars Part V)]. There doesn't seem to be any consensus on how to define "function" although there's general agreement on using sequence conservation as a first step. If some sequence under investigation is conserved in other species then that's a good sign that it's under negative selection and has a biological function. What if it's not conserved? Does that rule out function? The correct answer is "no" because one can always come up with explanations/excuses for such an observation. We discussed the example of de novo genes, which, by definition, are not conserved.Let's look at another example: splice variants. Splice variants are different forms of RNA produced from the same gene. If they are biologically relevant then they will produce different forms of the protein (for protein-coding genes). This is an example of alternative splicing if, and only if, relevance has been proven.
Tuesday, December 06, 2016
The term "function wars" refers to debates over the meaning of the word "function" in biology. It refers specifically to the discussion about junk DNA because junk DNA is defined as DNA that does not have a biological function. The wars were (re-)started when the ENCODE Consortium decided to use a stupid definition of function in order to prove that most of our genome was functional. This prompted a number of papers attempting to create a more meaningful definition.None of them succeeded, in my opinion, because biology is messy and doesn't lend itself to precise definitions. Look how difficult it is to define a "gene," for example. Or "evolution."
Nevertheless, some progress was made. Dan Graur has recently posted a summary of the two most important definitions of function [What does “function” mean in the context of evolution & what absurd situations may arise by using the wrong definition?]. The two definitions are "selected-effect" and "causal-role" (there are synonyms).
Humans have about 25,000 genes. About 20,000 of these genes are protein-coding genes.1 That means, of course, that humans make at least 20,000 proteins. Not all of them are different since the number of protein-coding genes includes many duplicated genes and gene families. We would like to know how many different proteins there are in the human proteome.The latest issue of Science contains an insert with a chart of the human proteome produced by The Human Protein Atlas. Publication was timed to correspond with release of a new version of the Cell Atlas at the American Society of Cell Biology meeting in San Francisco. The Cell Atlas maps the location of about 12,000 proteins in various tissues and organs. Mapping is done primarily by looking at whether or not a gene is transcribed in a given tissue.
A total of 7367 genes (60%) are expressed in all tissues. These "housekeeping" genes correspond to the major metabolic pathways and the gene expression pathway (e.g. RNA polymerase subunits, ribosomal proteins, DNA replication proteins). Most of the remaining genes are tissue-specific or developmentally specific.
Monday, December 05, 2016
There weren't many science writers are the Royal Society meeting in London (UK) [New trends in evolutionary biology: biological, philosophical and social science perspectives]. Carl Zimmer was there and so was Suzan Mazur. Carl was there to learn and do some research. Suzan was there to promote herself as the main publicist of the paradigm shifters.Carl Zimmer wrote a news article about the meeting for Quanta: Scientists Seek to Update Evolution. The subtitle was "Recent discoveries have led some researchers to argue that the modern evolutionary synthesis needs to be amended." It was a pretty fair article and pretty good reporting on what went on at the meeting. I would have been a bit more harsh about the success of the so-called "paradigm shifters" but Carl did a good job of conveying the skepticism exhibited by many at the meeting. [See Kevin Laland's new view of evolution for my take on these "revolutionaries."]
Sunday, December 04, 2016
The recent meeting at the Royal Society in London was organized by The Royal Society (UK) and The British Academy. The theme of the meeting was, "New trends in evolutionary biology: biological, philosophical and social science perspectives." The main organizers were Denis Noble, Nancy Cartwright, Patrick Bateson, John Dupré, and Kevin Laland. The point of the meeting was to discuss new evolutionary theory.It's difficult to describe everything that went on at the meeting because so much of it was details about individual research results. These scientific talks were often presented as an alternative to modern ways of thinking about evolution. The general theme was that the Modern Synthesis was out-of-date and needed revision or, perhaps, replacement. There was very little discussion of evolutionary theory and how best to interpret those results. The data was supposed to speak for itself.
The only serious objections came from scientists who claimed the Modern Synthesis had already incorporated the ideas of niche construction, plasticity, epigenetics etc. This message was promoted mainly by Douglas Futuyma and Russell Lande. They weren't very successful.
Thursday, December 01, 2016
Many evolutionary biologists are engaged in research that focuses on large organisms that are (presumably) adapting to a local environment. These "field biologists" are mostly concerned with rapid evolutionary changes. Those kind of changes are almost always due to natural selection. Many of these biologists are not interested in molecular evolution and not interested in any process other than natural selection.Unfortunately, this promotes an adaptationist mentality where all of evolution is viewed through the filter of natural selection. This is the view criticized by Stephen Jay Gould and Richard Lewontin back in 1978 when they presented the Spandrels paper at a Royal Society meeting in London (UK).
Gould, S. J. and Lewontin, R.C. (1979) The Spandrels of San Marco and the Panglossian Paradigm: A Critique of the Adaptationist Programme. Proc. R. Soc. Lond. B 205:581-598. [doi: 10.1098/rspb.1979.0086I believe there was a substantive change in our view of evolution back in the late 1960s and early 1970s. That's when the results of evolution at the molecular level were first being published. It lead to the development of Neutral Theory, Nearly-Neutral Theory and a growing appreciation of the importance of random genetic drift. Modern population genetics was able to cope easily with this new view of evolution.
Monday, November 21, 2016
Many science writers complain about the ability of scientists to explain their work to the general public. The latest example is from Susan Matheson, a science writer with a Masters degree in industrial engineering from Rutgers University (New Jersey, USA). She published the following article in Cell a leading journal in the field of cell biology, biochemistry, and molecular biology.
A Scientist and a Journalist Walk into a Bar…Mathesons begins with an anecdote about a science writer who won a Pulitzer Prize in 2011 for writing about a 4-year-old boy with a rare genetic disease. She concludes,
by Susan Matheson, Cell 167: 1140–1143 (2016)[doi: 10.1016/j.cell.2016.10.051] [ScienceDirect PDF] [link from Susan Matheson]
Who are science journalists, and how can journalists and research scientists work together to improve science communication?
Wednesday, October 19, 2016
This is our first visit to Scotland. We rented an apartment in the top floor of this house in the middle of the city. It's a 20 minute walk to the port (Leith) and about the same distance to the old city (Edinburgh).
We'll be staying for two weeks in Scotland.
Our first meal in Scotland was at a pub in "the shore" near the main port.
Monday, October 17, 2016
I will be attending the Royal Society Meeting on New trends in evolutionary biology: biological, philosophical and social science perspectives. I'll post each of the abstracts and ask for your help in deciding what question to pose to the speakers. Here's the abstract for Melinda Zeder's talk on Domestication: a model system for evolutionary biology.
In his book The Variation of Animals and Plants under Domestication Darwin used domestication as a model system to explore his theories about the role of natural selection in evolution. Gregor Mendel used peas to trace the rules of heredity that formed the basis of the science of genetics, and that, when combined with Darwinian evolution, formed the basis of the Modern Synthesis. It seems only appropriate for domestication to serve once again as a model system for assessing how recent insights into the role of multiple shaping processes and forms of inheritance can be incorporated into an extended understanding of evolution. This presentation explores the value of domestication in evaluating core assumptions that differentiate the classical Modern Synthesis and the Extended Evolutionary Synthesis including: 1. reciprocal causation, 2. developmental processes as drivers of evolutionary change, 3. inclusive inheritance, and 4. the tempo and rate of evolutionary change.Melinda Zeder works at the National Museum of Natural History, Smithsonian Institution (USA). I think I'll ask her what domestication teaches us about the fixation of deleterious alleles by random genetic drift and how that fits into Darwin's ideas and her view of the Modern Synthesis.
I will be attending the Royal Society Meeting on New trends in evolutionary biology: biological, philosophical and social science perspectives. I'll post each of the abstracts and ask for your help in deciding what question to pose to the speakers. Here's the abstract for Susan Antón's talk on Human evolution, niche construction and plasticity.
Recent humans are biocultural organisms. Our worldwide distribution and status as the lone surviving species of our genus signal a level of evolutionary success often explained by both biological and cultural mechanisms. A bio-behavioural package of traits that co-exist in Homo sapiens, including large brains and bodies, small teeth and jaws, extensive cooperative care, a great deal of developmental plasticity, and an extensive amount of niche construction, are variously implicated in our success or seen as its result.Susan Antón is a professor of anthropology at New York University (New York, NY, USA).
It is broadly accepted that recent humans are ‘different’, particularly in the extent of our cultural interventions, than our earlier hominin forebears. But whether this is a difference in kind or degree, how far back that difference stretches, and whether those outcomes modifiable over an individual’s lifetime are important to human evolution is open to debate. Regardless of whether we accept exogenetic changes – including developmental niche construction – as consistent with an extension of, or break with the evolutionary synthesis, Homo erectus has often been proposed as the locus at which more ‘human like’ modes of behaviour (and presumably more biocultural evolution) is seated. But the paucity of the fossil record and the tenuously established links between bones and behaviours of interest limit our ability to test these assertions. I review the evolution of Homo and recent attempts to locate the transition to a biocultural organism with new data and by both working back from recent humans through archaeological time and working forward from ancestral genera.
It's interesting to learn about the history of life and the evolution of a particular species. However, that specific history usually doesn't usually have much impact on evolutionary theory. I wonder if some speakers are confused about the relationship between studying the history of life and the big picture of evolutionary theory? I fail to see how this study translates to a deeper understanding of the evolution of mushrooms, maple trees, and microbacteria.
I will be attending the Royal Society Meeting on New trends in evolutionary biology: biological, philosophical and social science perspectives. I'll post each of the abstracts and ask for your help in deciding what question to pose to the speakers. Here's the abstract for Andrew Whiten's talk on A second inheritance system: the extension of biology through culture.
By the mid-twentieth century the behavioural sciences could offer only the sketchy beginnings of a scientific literature documenting evidence for cultural inheritance in animals – the transmission of traditional behaviours via imitation and other processes of learning from others (social learning). By contrast, recent decades have seen a massive growth in the documentation of such cultural phenomena, driven by long-term field studies and complementary laboratory experiments. Here I first offer an overview of the major discoveries in this field, which increasingly suggest that this ‘second inheritance system’, built on the shoulders of the primary genetic inheritance system, occurs widely amongst vertebrates and possibly in insects and other invertebrates too. Its novel characteristics suggest it should have major implications for our understanding of evolutionary biology. Two major questions arising are accordingly addressed. One concerns the extent to which this second system echoes or differs from the principal properties of the primary evolutionary system described in the neo-Darwinian synthesis of the twentieth century and its extensions under discussion at this meeting. A subsidiary issue here is how the answers may differ much according to whether the focus is on the massively cumulative cultural evolution distinctive of our own species, or on the forms of cultural transmission documented for other species. The second major, and related, question concerns the extent to which the new discoveries about animal cultural transmission extend evolutionary theory, either in addition to or through interaction with the primary, genetically based inheritance systems.Andrew Whiten is an emeritus professor in the School of Psychology and Neuroscience at the University of St. Andrews (Scotland, UK). I'm curious to see his explanation of how cultural evolution in, say, bonobos, informs us about biological evolution.
Here's a possible question ...
The people living in St. Andrews experience a very different culture than the people living in the suburbs of Dallas, Texas. Both groups have been exposed to Donald Trump since he owns a golf club near St. Andrews but they are likely to react differently to Trump. How will these cultural differences affect the biological evolution of the two groups in Texas and Scotland?
I will be attending the Royal Society Meeting on New trends in evolutionary biology: biological, philosophical and social science perspectives. I'll post each of the abstracts and ask for your help in deciding what question to pose to the speakers. Here's the abstract for Agustín Fuentes' talk on
Human niche, human behaviour, human nature.
Scholars from a diverse range of disciplines disagree on what human nature is, what it could be, or even if there is one. There is no single ‘best’ discourse on, or mode of approach to, human nature. However, in the context of what we know about the evolutionary history, anthropology, and biology of Homo sapiens sapiens it is clear that an evolutionary approach should be among the principal modes of inquiry. At present we are faced with a few different narratives as to exactly what such an evolutionary approach entails. However, one point is clear: we need a robust and dynamic theoretical toolkit in order to develop a richer, and more nuanced, understanding of the cognitively sophisticated genus Homo and the diverse sorts of niches humans constructed and occupied across the Pleistocene, Holocene, and into the Anthropocene. In this talk I review current evolutionary approaches to ‘human nature’ and argue that we benefit from re-framing our investigations via the concept of the human niche and in the context of the Extended Evolutionary Synthesis (EES). In providing an overview of human evolution and the human niche I illustrate the benefits of moving the discourse on human nature(s) to an integrated evolutionary approach incorporating processes of the Extended Evolutionary Synthesis. This is not a replacement of earlier evolutionary approaches but rather an expansion and enhancement, a broadening of our toolkit and the landscape of inquiry. I offer brief examples from human evolutionary histories in support of these assertions.Agustín Fuentes is a professor of anthropology at the University of Notre Dame in Indiana (USA). This is another talk about the nature of "human nature." Since I'll probably be skipping the previous talk I'll likely stay in some pub until this one is over. Looking forward to a "full English."
I will be attending the Royal Society Meeting on New trends in evolutionary biology: biological, philosophical and social science perspectives. I'll post each of the abstracts and ask for your help in deciding what question to pose to the speakers. Here's the abstract for Tim Lewens' talk on Human nature, human culture: the case of cultural evolution.
In recent years, far from arguing that evolutionary approaches to our own species permit us to describe the fundamental character of human nature, a prominent group of cultural evolutionary theorists has instead argued that the very idea of 'human nature' is one we should reject. It makes no sense, they argue, to speak of human nature in opposition to human culture. But the very same sceptical arguments have also led some thinkers – usually from social anthropology – to dismiss the related idea that we can talk of human culture in opposition to human nature.Tim Lewens is a professor in the Department of the History and Philosophy of Science at the University of Cambridge (UK). I'm not the least bit interested in cultural evolution (i.e. history) and I'm certainly not interested in quibbling about the meaning of "human nature." I hope there's a good pub nearby 'cause I'm going to skip this talk.
How, then, are we supposed to understand the cultural evolutionary project itself, which seems to rely on a closely allied distinction between 'organic' and 'cultural' evolution? This talk defends the cultural evolutionary project against the charge that, in refusing to endorse the concept of human nature, it has inadvertently sabotaged itself.
Tuesday, October 11, 2016
I will be attending the Royal Society Meeting on New trends in evolutionary biology: biological, philosophical and social science perspectives. I'll post each of the abstracts and ask for your help in deciding what question to pose to the speakers. Here's the abstract for Karola Stotz's talk on
Developmental niche construction.
In the last decade niche construction has been heralded as the neglected process in evolution. But niche construction is just one way in which the organism’s interaction with, and construction of the environment, can have potential evolutionary significance. This constructed environment not just selects for, it also produces new variation. Nearly three decades ago, and in parallel with Odling-Smee’s book chapter ‘Niche-constructing phenotypes’, West and King introduced the ‘Ontogenetic Niche’ to give the phenomena of exogenetic inheritance a formal name. Since then a range of fields in the life sciences and medicine has amassed evidence that parents influence their offspring by means other than DNA (parental effects). Diverse scientists use different theoretical constructs for overlapping sets of processes, all of which show one way or another how heritable variation can be environmentally induced and developmentally regulated. Here I propose the concept of ‘developmental niche construction’ as a framework to integrate findings from fields ranging from molecular biology to developmental psychology. It elucidates how a diverse range of mechanisms contributes to the transgenerational transfer of developmental resources. This talk will explore the overall significance of these developments in the life sciences, and particularly how they advance the ongoing integration of development, heredity, ecology, and evolution.Karola Stotz is a philosopher at Macquarie University in Sydney, Australia.
Organisms interact with, and change, their environment. This is hardly news but it's being promoted as one of the "new trends in evolutionary biology." Why?
I think I'll ask her what's "new" about this?
I will be attending the Royal Society Meeting on New trends in evolutionary biology: biological, philosophical and social science perspectives. I'll post each of the abstracts and ask for your help in deciding what question to pose to the speakers. Here's the abstract for Samir Okasha's talk on
Evolution and the metaphor of agency.
It is striking that evolutionary biology often uses the language of intentional psychology to describe the behaviour of evolved organisms, their genes, and the process of natural selection that led to their evolution. Thus a cuckoo chick ‘deceives’ its host; a worker ant ‘prefers’ to tend the queen's eggs to those of other workers; a swallow ‘realises’ that winter is approaching and ‘wants’ to escape it; an imprinted gene ‘knows’ whether it was inherited paternally or maternally; and natural selection ‘chooses’ some phenotypes over others.Samir Okasha is a professor of philosophy at the University of Bristol (UK). He raises an interesting point but it's a very old point that has been discussed and resolved many years ago. I don't think this has anything to do with extending evolutionary theory. It doesn't even count as a "new trend in evolutionary biology" (the title of the conference).
This intentional idiom is a symptom of a broader way of thinking about and modelling evolution, which I call ‘agential’. This involves treating evolved entities, paradigmatically individual organisms, as if they were agents trying to achieve a goal, namely maximisation of reproductive fitness (or some proxy). The use of rational choice models, originally intended to apply to deliberate human action, in an evolutionary context, is one symptom of agential thinking.
I offer a cautious defence of agential thinking in evolutionary biology. I argue that this mode of thinking does genuine intellectual work, and is not ‘idle metaphor’. The key point is that attributions of agency presuppose a ‘unity of purpose’. Therefore an evolved organism can only be treated as agent-like to the extent that its phenotypic traits have complementary rather than antagonistic functions, i.e. contribute to a single overall goal. Where this is not the case, e.g. because of unresolved intra-genomic conflict, the metaphor of agency ceases to be applicable.
Friday, October 07, 2016
The Lawrence Berkeley National Laboratory employs a number of scientists who work on genes and gene expression. Here's part of a press release published two days ago [For Normal Heart Function, Look Beyond the Genes: Loss of noncoding elements of genome results in heart abnormalities, finds Berkeley Lab study]. It demonstrates that the workers at this National Laboratory don't understand anything about mammalian genomes.The only other possibility is that the person who wrote the press release doesn't understand molecular biology1 and the scientists who work there just don't care what their institution publishes.
Researchers have shown that when parts of a genome known as enhancers are missing, the heart works abnormally, a finding that bolsters the importance of DNA segments once considered “junk” because they do not code for specific proteins.Regular readers of this blog know that ...
- No knowledgeable scientist ever said that all noncoding DNA was junk.
- We've known about regulatory sequences for half a century. We've known about enhancers—just another kind of regulatory sequence—for thirty-five years. Nobody ever thought they were junk. Nobody ever thought they were unimportant.
When scientists sequenced the human genome, they discovered that less than 5 percent of our DNA were genes that actually coded for protein sequences. The biological functions of the noncoding portions of the genome were unclear.At some point this flagrant misrepresentation of facts must be stopped. It's hurting science.
Over the past fifteen years, however, there has been a growing appreciation for the importance of these noncoding regions, thanks in large part to the efforts of individual labs and, more recently, large international efforts such as the Encyclopedia of DNA Elements (ENCODE) project.
What became clear from this work is that there are many elements of the genome, including enhancers, that are involved in regulating gene expression, even though they do not encode for proteins directly.
How can you believe anything in the press release once you read this? Do you think this represents the views of the scientists who published the paper? Is so, shame on them. If not, shame on the Lawrence Berkeley National Laboratory.
1. I sent her a link to this post.
Tuesday, October 04, 2016
I will be attending the Royal Society Meeting on New trends in evolutionary biology: biological, philosophical and social science perspectives. I'll post each of the abstracts and ask for your help in deciding what question to pose to the speakers. Here's the abstract for Patrick Bateson's talk on Adaptability and evolution.
The capacity of organisms to respond in their own lifetimes to new challenges in their environments probably appeared early in biological evolution. At present few studies have shown how such adaptability could influence the inherited characteristics of an organism’s descendants. Nevertheless such effects on biological evolution are likely to have been important and when they occurred accelerated the pace of evolution. Ways in which this might have happened have been suggested many times since the 1870s. I shall review these proposals and discuss their relevance to modern thought.I don't get it. A key example of organisms responding to their environment is transcription of the lac operon in E. cloi. How does regulation of the lac operon accelerate evolution?
Part of the confusion here is that Bateson is using "adaptability" in two different senses. I'm curious to see if he makes this distinction clear in his talk.
I don't see anything new or revolutionary here. Apparently his motive isn't to overthrow or extend evolutionary theory but to introduce evolution to nonscientists. Here's what he said in an interview with Suzan Mazur [Sir Patrick Bateson: Zoologists Should Not ‘Hog’ Upcoming Royal Society Evolution Meeting ...
Patrick Bateson: It may be a mistake not to have anybody talking about that specifically at the meeting. But I want to repeat that in organizing the meeting we are focused on a discussion about evolution with our colleagues in the social sciences and the humanities, and we don’t want to blind them with all the details of the sciences.I don't know who's going to be at the meeting but I don't see very many molecular biologists or population geneticists among the speakers. It's mostly zoologists and a few philosophers.
There’s also a lot of fascinating work going on in population genetics that we’re not going to talk about. Evolutionary biologists will say this is an important part of evolutionary biology, which it is, of course. But it isn’t relevant to this particular meeting.
Suzan Mazur: How will an evolution paradigm shift affect society in general?
Patrick Bateson: I’m not sure we’re going to be talking about a completely new set of ideas, a lot have been around for a while. Frankly, I think some evolutionary biologists have not shed their neo-Darwinist clothing. There are some conservative-minded biologists who still think of the organism as being essentially passive, a view about which I am particularly concerned. However, the overall movement in biology is to integrate different disciplines making it a very lively area at the moment. The molecular biologists are talking to the ethologists, the ecologists to the physiologists, the population geneticists to the paleontologists, and so forth.
I will be attending the Royal Society Meeting on New trends in evolutionary biology: biological, philosophical and social science perspectives. I'll post each of the abstracts and ask for your help in deciding what question to pose to the speakers. Here's the abstract for Andy Gardner's talk on Anthropomorphism in evolutionary biology.
A longstanding tension exists in evolutionary biology between behavioural ecology – in which organisms are treated as having adaptive, fitness-maximising agendas; and population genetics – in which such notions are decried as naïve ‘anthropomorphism’ and are widely rejected. I explore the formal and scientific justification for evolutionary anthropomorphism and consider its application to the understanding of adaptive design at the level of genes, individuals and societies.Andy Gardner is a biologist at the University of St. Andrews in Scotland (UK). Here's a description of his research interests from his website.
I work on Darwinian adaptation. Natural selection explains the appearance of design in the living world, but at what level is this design expected to manifest – gene, individual, society – and what is its function? Social evolution provides a window on this problem, by pitting the interests of genes, individuals and societies against each other. I develop general theory on the topics of inclusive fitness and multilevel selection, and also tailor general theory to the biology of particular species to facilitate empirical testing. I work on a wide range of biological systems, including viruses, bacteria, protozoa, crustaceans, insects, fish and humans.I'm not sure how this view differs from Gould's writings on hierarchical theory. I'm looking forward to hearing the answer.
Sunday, October 02, 2016
I will be attending the Royal Society Meeting on New trends in evolutionary biology: biological, philosophical and social science perspectives. I'll post each of the abstracts and ask for your help in deciding what question to pose to the speakers. Here's the abstract for Denis Noble's talk on Evolution viewed from medicine and physiology.
Medicine and physiology are multi-level disciplines. So is physics. From physics we learn that ordered properties at high levels co-exist with randomness at lower levels. Molecules in organisms must obey the same principles. Stochasticity at low levels does not therefore exclude order at higher levels. Organisms enlist stochasticity in their development of functional behaviour, through restraints exerted by higher over lower levels. The physics of organisms must therefore interact with their genomes to produce the phenotype1,2. Reverse engineering from physiological models is then required to understand genotype-phenotype relations3. There is no privileged level of causality4, nor privileged level of selection5. Evolution involves interaction between several processes at multiple levels, as Charles Darwin also believed5,6. Without understanding these interactions, gene-centred approaches will continue to produce disappointing results in healthcare7,8, including trans-generational disease risks.I have heard Denis Noble speak and I've read some of his papers [Physiologists fall for the Third Way; A physiologist thinks about evolution]. Denis Noble is a physiologist who worked on hearts and circulation in complex mammals (humans). He's very annoyed at biochemists and molecular biologists for getting so much attention (and money) over the past few decades. He has constructed in his mind a false image of evolution. He thinks it's entirely adaptationist and gene-centric and that's what he rails against. He doesn't like Richard Dawkins. He's a prominent member of The Third Way.
You can see for yourself by watching a video of a talk he gave a few years ago.
I agree completely with Jerry Coyne's analysis of this talk [Famous physiologist embarrasses himself by claiming that the modern theory of evolution is in tatters]. Jerry says ....
I’m writing this post in a bit of anger, as Noble’s attacks on the modern synthesis are both poorly informed and clearly motivated by his ambition to make physiology a central part of evolutionary biology. Although he’s an FRS and famous, he wants more: he wants his field to be central to evolution. But such misguided hubris is not the way science is supposed to be done. And physiology is already important in evolutionary biology. It’s the reason why we look at the effects of a gene substitution, for example, not as a simple one-gene-produces-one-trait issue, but as a the gene’s overall effect on reproductive output through its effects ramifying through the complexities of development. Noble says that evolutionists are guilty of this “one-gene-one-trait” error, but he’s just wrong: I don’t know a single person in my field who holds this simplistic view.I'm not going to ask any questions after this talk. I'll report back on how many people seem to agree with him.
None of the arguments that Noble makes are new: they’re virtual tropes among those people, like James Shapiro and Lynn Margulis, who embarked, at the end of their careers, on a misguided crusade to topple the modern theory of evolution.
However famous Noble may be in physiology, he’s a blundering tyro when it comes to evolutionary biology. He might try discussing his ideas with other evolutionists and listening to their responses. He obviously hasn’t done that, and yet travels the world trading on his expertise in physiology to show that the edifice of modern evolutionary biology is rotten. And he writes papers to that effect, including the dreadful piece referenced below.
But what’s really rotten is Noble’s knowledge of the field and his claim that virtually every assumption of neo-Darwinian evolution is wrong. In fact, his arguments are so rotten that they stink like old herring.
They’re not even wrong.
I will be attending the Royal Society Meeting on New trends in evolutionary biology: biological, philosophical and social science perspectives. I'll post each of the abstracts and ask for your help in deciding what question to pose to the speakers. Here's the abstract for Eva Jablonka's talk on
The role of epigenetic inheritance in evolution.
The construction of the ‘Modern Evolutionary Synthesis’ in the mid-twentieth century involved the exclusion of soft inheritance – the inheritance of the effects of developmental modifications – and, by implication, the possibility of any form of ‘Lamarckian’ evolution. However, in later decades, discoveries of molecular mechanisms that can support such inheritance led to a broadening of the notion of biological heredity. After discussing the historical context in which this change occurred, I present an extended notion of inheritance, focusing on epigenetic inheritance and its underlying mechanisms. I examine the evidence for the ubiquity of epigenetic inheritance, present models of population epigenetics, and discuss the involvement of epigenetic inheritance in adaptive evolutionary change and macro-evolution. I argue that considering the many evolutionary consequences of epigenetic inheritance requires an extension of the evolutionary synthesis beyond the current neo-Darwinian model.Eva Jablonka has been pushing the importance of epigenetics for many years. Here's a video where she explains why epigenetic inheritance needs to be incorporated into evolutionary theory.
I think she's exaggerating the importance of epigenetic inheritance in evolution. I'd like to ask her how she defines "epigenetics" and how much of it is heritable over enough generations to seriously affect the evolution of a population. I'm particularly interested in her claim that epigenetic inheritance affects macro-evolution.
Saturday, October 01, 2016
I will be attending the Royal Society Meeting on New trends in evolutionary biology: biological, philosophical and social science perspectives. I'll post each of the abstracts and ask for your help in deciding what question to pose to the speakers. Here's the abstract for Paul Griffiths's talk on Genetic, epigenetic and exogenetic information in development and evolution.
I outline an approach to measuring biological information where ‘information’ is understood in the sense found in Francis Crick’s foundational contributions to molecular biology. Genes contain information in this sense, but so do epigenetic factors, as many biologists have recognised. The term ‘epigenetic’ is ambiguous, and I introduce a distinction between epigenetic and exogenetic inheritance to clarify one aspect of this ambiguity. These three heredity systems play complementary roles in development and evolution.Paul Griffiths is a philosopher of biology from Australia. He has been interested in genes for many years. I don't know what he's going to say about epigenetics. I suspect he can make a case for information in the sense that a naked DNA sequence differs in information from a methylated DNA sequence. (Restriction/modification is a good example.)
The problem with this kind of hair splitting is that ultimately the extra information (e.g. methylation) is provided by enzymes (methylases) encoded by genes in the genome. Epigenetics, per se, doesn't add any new information. It's just a consequence, or outcome, of the information already in the DNA.
I will be attending the Royal Society Meeting on New trends in evolutionary biology: biological, philosophical and social science perspectives. I'll post each of the abstracts and ask for your help in deciding what question to pose to the speakers. Here's the abstract for James Shapiro's talk on Biological action in Read-Write genome evolution.
Many of the most important evolutionary variations that generated phenotypic adaptations and originated novel taxa resulted from complex cellular activities affecting genome content and expression. These activities included: (i) the symbiogenetic cell merger that produced the mitochondrion-bearing ancestor of all extant eukaryotes; (ii) symbiogenetic cell mergers that produced chloroplast-bearing ancestors of photosynthetic eukaryotes; and (iii) interspecific hybridisations and genome doublings that have generated adaptive radiations and new species of higher plants and animals. Adaptive variations have also arisen by horizontal DNA transfers (frequently involving infectious agents), by natural genetic engineering of coding sequence DNA in protein evolution (e.g. exon shuffling), and by mobile DNA rewiring of transcriptional regulatory networks, such as those essential to viviparous reproduction in mammals. In the most highly evolved multicellular organisms, we now know that biological complexity scales with ‘non-coding’ DNA content rather than with protein-coding capacity in the genome. Coincidentally, we have come to recognise that ‘non-coding’ RNAs rich in repetitive mobile DNA sequences function as key regulators of complex adaptive phenotypes, such as stem cell pluripotency. The intersections of cell activities and Read-Write genome modifications provide a rich molecular and biological foundation for understanding how ecological disruptions can stimulate productive, often abrupt, evolutionary transformations.I have dozens of questions for Jim Shapiro but here are two possibilities.
Most of the events you describe are one-off events in the history of life. They are mostly accidents. They were unpredictable. How does the occurrence of unique events such as endosymbiosis or genome doubling fit into evolutionary theory as opposed to just historical facts in the history of life.
Michael Lynch and others say that the amount of junk DNA in a genome correlates with the population size of the species. This view is perfectly consistent with modern population genetics. There is plenty of evidence that 90% of our genome is junk. You seem to be implying that this extra DNA is not junk but serves some adaptive purpose. What evidence do you have that supports this claim and why do you disagree with Michael Lynch?
I will be attending the Royal Society Meeting on New trends in evolutionary biology: biological, philosophical and social science perspectives. I'll post each of the abstracts and ask for your help in deciding what question to pose to the speakers. Here's the abstract for Kevin Laland's talk on The middle ground between artificial and natural selection: niche construction as developmental bias.
Organisms modify and choose components of their local environments. This ‘niche construction’ is subject to extensive research across several academic fields. It is well appreciated that niche construction can alter ecological processes, modify natural selection, and contribute to inheritance through ecological legacies. However, niche construction is not usually regarded as an evolutionary process, probably because traditional evolutionary accounts restrict evolutionary processes to phenomena that directly change gene frequencies (e.g. selection, mutation, drift).I don't get this emphasis on niche construction. Biologists have been talking about how organisms modify the environment for one hundred years or more. I can see how an understanding of particular examples, such as the increase in oxygen levels due to the evolution of water splitting reactions, can provide insight into the history of life but how does that fit into evolutionary theory?
Alternative perspectives can be of value if they generate novel predictions, open up new lines of enquiry, or generate new insights. The niche-construction perspective within evolutionary biology provides an alternative account of the causal relations underlying adaptation, a stance that has already led to a number of valuable insights. Here I suggest that there is heuristic value in regarding niche construction as an evolutionary process, on the grounds that it initiates and modifies the selection acting back on the constructor (and other species) in an orderly and directional manner. As a consequence, niche construction co-directs adaptive evolution by imposing a statistical bias on selection (an externally expressed form of developmental bias).
I illustrate how niche construction can generate developmental bias by comparing it with artificial selection, where I suggest it occupies the middle ground between artificial and natural selection. This perspective has heuristic value for the evolutionary biologist, leading to testable predictions related to: (i) trait evolution, including the evolution of sequences of traits and parallel evolution; (ii) responses to natural selection in the wild; and (iii) biodiversity.
I don't have any questions for Kevin Laland. I'm anxious to see how the people at this meeting view niche construction.
I will be attending the Royal Society Meeting on New trends in evolutionary biology: biological, philosophical and social science perspectives. I'll post each of the abstracts and ask for your help in deciding what question to pose to the speakers. Here's the abstract for Paul Brakefield's talk on Does the way in which development works bias the paths taken by evolution?
Developmental bias was defined in a seminal review some thirty years ago that resulted from an early ‘meeting of minds’ of developmental and evolutionary biologists driven by John Maynard Smith and Lewis Wolpert. Although there has been dramatic progress since then in revealing in exquisite detail how morphologies develop, there are few well-worked case studies of potential developmental bias, as well as little understanding of how important the process has been in shaping the evolution of animal form. Therefore, it is timely to think about what is needed to facilitate the analysis of the extent to which patterns of evolutionary diversification are biased by how development works, and indeed whether it is useful to distinguish this process from that of genetic channeling.Here are two possible questions for Paul Brakefield ...
Stephen Jay Gould published Ontology and Phylogeny in 1977. He wrote extensively about developmental constraints until his death in 2002. Richard Dawkins also wrote about developmental constraints, most notably in his discussion of whether pigs could fly in The Blind Watchmaker. How do your views differ from those that have been around for decades and why do you think it requires a modification of evolutionary theory today?
In The Structure of Evolutionary Theory, Gould wrote 270 pages on developmental constraints emphasizing their POSITIVE role in evolution as opposed to just their negative effects on limiting natural selection. He said,
The concept of constraint must include theoretically legitimate and factually important positive meanings—i.e., constraints as directing causes of particular evolutionary changes—rather than only the negative connotations of structural limitations that prevent natural selection from crafting an alteration that would otherwise be favored and achieved.How do your views differ from what Gould wrote about so extensively in 2001?
I will be attending the Royal Society Meeting on New trends in evolutionary biology: biological, philosophical and social science perspectives. I'll post each of the abstracts and ask for your help in deciding what question to pose to the speakers. Here's the abstract for John Dupré's talk on The ontology of evolutionary process.
Ontology is the branch of philosophy that considers in the most general way the nature of reality. An ancient and fundamental ontological question is whether reality is ultimately composed of stable things or is everywhere processual, in flux. A number of distinguished 20th century biologists, including, for instance Conrad Waddington, Joseph Needham, and Ludwig von Bertalanffy, thought it important to stress the fundamentally dynamic, processual character of living systems. While evolution is of course a process, it is often implicitly supposed that the entities that evolve or that constitute the evolutionary process, whether genes, organisms, populations, or whatever, are kinds of things. Following the authors mentioned above, I argue that these too are better seen as processes, albeit highly stabilised processes.John Dupré is a philosopher. He talks like a philosopher. I don't understand what he's talking about and, quite frankly, I don't care. No questions for him.
In this talk I shall argue that a process ontology is correct and that it has important implications for how we should think about evolution. First, with regard to the constituents of the evolutionary process, process ontology highlights the limitations of atemporal descriptions of organisms, for example in terms of gene sequence, and of populations as atemporal abstractions from evolving lineages. Second, whereas in an ontology of things the primary explanatory task is that of understanding change, in a world of process it is of equal or even greater importance to explain stability. The first step in articulating a fully processual view of evolution is to describe the processes that sustain persisting lineages. Doing so should provide fresh perspectives on the processes that can produce changes in lineages.
Friday, September 30, 2016
I will be attending the Royal Society Meeting on New trends in evolutionary biology: biological, philosophical and social science perspectives. I'll post each of the abstracts and ask for your help in deciding what question to pose to the speakers. Here's the abstract for Tobias Uller's talk on Heredity and evolutionary theory.
Heredity is a central concept in biology and one of the core principles needed for evolution by natural selection. For most of the past century inheritance has been conceptualised and defined in terms of transmission of genes. Emerging developmental perspectives on evolution appear to challenge this perspective in several ways. Here I will explain how evolutionary biologists treat heredity conceptually and mathematically. These perspectives are heuristically useful but they impose a certain structure on evolutionary theory and leave out aspects of heredity that may be important to understand evolution. An alternative representation understands heredity as an outcome of developmental processes. I will suggest that this perspective helps to clarify how different mechanisms of inheritance contributes to evolution.I have to wait to hear this talk in order to figure out what he means. From reading the abstracts to some of his papers I think he's going to promote plasticity and epigenetics ... or maybe maternal effects.
In any case, the standard understanding of "heredity" is when alleles (genes) are passed from one generation to another. The process usually involves DNA replication and cell division but it encompasses horizontal transmission. I'll be interested in hearing about other mechanisms of heredity.
I will be attending the Royal Society Meeting on New trends in evolutionary biology: biological, philosophical and social science perspectives. I'll post each of the abstracts and ask for your help in deciding what question to pose to the speakers. Here's the abstract for Russell Lande's talk on Evolution of phenotypic plasticity.
The scope and relative rates of adaptive phenotypic change from plasticity versus standard Darwinian evolution adaptive genetic changes depend on the time scale and the range of phenotypic alteration being considered. This distinction becomes blurred when plasticity itself evolves. Using standard methods from neo-Darwinian population genetic theory, I review recent models on the evolution of phenotypic plasticity in changing environments, emphasising the roles of environmental predictability and costs of plasticity in constant and labile characters. Adaptation to a novel environment may often occur by rapid evolution of increased plasticity followed by slow genetic assimilation of the new phenotype. I elucidate the connection between environmental tolerance and plasticity. The theory of evolution of phenotypic plasticity is an important extension to neo-Darwinism, but does not necessitate a major revision of its foundations. The same conclusion applies to epigenetic mechanisms including interactions between genes or tissues in development, and to transgenerational phenotypic effects such as somatic inheritance, maternal effects and DNA methylation.I could ask this question ...
Imagine a small group of organisms that find themselves in a new environment. Let's assume they have a genome containing 10,000 genes. How do they select for increased phenotypic plasticity in order to better adapt to the new environment? Are all genes affected or just a small number that might increase fitness? Which genes acquire additional potentially beneficial alleles that were not present in the small population before it encountered the new environment and how does that mechanism work?
I will be attending the Royal Society Meeting on New trends in evolutionary biology: biological, philosophical and social science perspectives. I'll post each of the abstracts and ask for your help in deciding what question to pose to the speakers. Here's the abstract for Sonia Sultan's talk on Developmental plasticity: re-conceiving the genotype.
For several decades, the phenotype of an organism (i.e, its traits and behaviour) has been studied as the outcome of developmental ‘instructions’ coded in its DNA. According to this model, each genotype is expressed as a specific phenotype; individual differences in fitness-related traits are seen to arise from this stably inherited internal information. This simplified view of development provides the foundation for a Modern Synthesis approach to adaptive evolution as a sorting process among genetic variants. As developmental biologists are aware, however, an organism’s phenotype is not strictly pre-determined by its genotype, but rather takes shape through the interplay of genetic factors with the organism’s environmental conditions. By means of this developmental plasticity, a given genotype may express different phenotypes under different environmental conditions. Accordingly, the genotype can be understood as a repertoire of potential developmental outcomes or norm of reaction.Here's a possible question ...
Re-conceiving the genotype as an environmental response repertoire rather than a fixed developmental programme leads to three critical insights, as illustrated by norm of reaction data from Polygonum plants. Plastic responses to specific conditions often comprise functionally appropriate trait adjustments, resulting in an individual-level, developmental mode of adaptive variation. Environmental responses can extend across generations via effects on progeny growth and fitness, a form of inherited yet non-genetic adaptation. Finally, because genotypes are differently expressed depending on the environment, the genetic diversity available to natural selection is itself environmentally contingent.
Back in the 1960s we learned that transcription of the lac operon in E. coli was regulated by the environment. This regulation, activation or repression, was passed on to daughter cells as the cells divided. Why didn't this discovery lead to a major revision of evolutionary theory?
I will be attending the Royal Society Meeting on New trends in evolutionary biology: biological, philosophical and social science perspectives. I'll post each of the abstracts and ask for your help in deciding what question to pose to the speakers. Here's the abstract for Douglas Futuyma's talk on The evolutionary synthesis today: extend or amend?
Evolutionary theory has been extended almost continually since the Evolutionary Synthesis, but the principal tenets of the Synthesis have been strongly supported, the single most important exception being the greater importance accorded genetic drift, especially in molecular evolution. The calls for an extended synthesis today are largely a continuation of this process. Some elements of the EES movement, such as the role of niche construction, are welcome emphases on long recognised but perhaps under-studied processes. The union of population genetic theory with mechanistic understanding of molecular and developmental processes is a potentially productive conjunction of ultimate and proximal causation; but the latter does not replace or invalidate the former. Newly discovered molecular genetic phenomena have been easily accommodated by orthodox evolutionary theory in the past, and this appears to hold also for phenomena such as epigenetic inheritance today. In several of these areas, empirical evidence is needed to evaluate enthusiastic speculation. Evolutionary theory today will continue to be extended, but there is no sign that it requires emendation.Here are two possible questions for Futuyma.
Why do you think that most participants at this meeting seem to be unaware of random genetic drift and the evolution of structures and phenotypes by nonadaptive processes? Doesn't this strike you as bizarre for a group that's so concerned about evolutionary theory?
As you explain in your textbook, describing the pathways to modern species contributes to the FACT of evolution and the FACT of descent with modification but how those genetic changes actually occur and become fixed is part of evolutionary theory. Do you distinguish between evolutionary theory and the actual history of life?
I will be attending the Royal Society Meeting on New trends in evolutionary biology: biological, philosophical and social science perspectives. I'll post each of the abstracts and ask for your help in deciding what question to pose to the speakers. Here's the abstract for Gerd B. Müller's talk on The extended evolutionary synthesis.
Since the last major conceptual integration in evolutionary biology – the Modern Synthesis of the 1940s – the biosciences have made significant advances. The rise of molecular biology and evolutionary developmental biology, the recognition of ecological development, niche construction and of multiple inheritance systems, the -omics revolution and the science of systems biology, among other developments, have provided a wealth of new knowledge regarding the mechanisms of evolutionary change. Some of these results are in agreement with the classical Synthetic Theory and others reveal different properties of evolutionary change. A renewed and extended evolutionary synthesis unites pertinent concepts emerging from these novel fields with elements from the standard theory, but it differs from the latter in its core logic and predictive capacities. Whereas the classical theory had concentrated on genes and adaptive variation in populations, the extended framework emphasises the role of constructive processes, environmental induction, and systems dynamics in the evolution of organismal complexity. Single level and unilinear causation is replaced by multilevel and reciprocal causation. Among other consequences, this entails a revised understanding of the role of natural selection in the evolutionary process. The extended evolutionary synthesis complements the traditional gene centric perspective and stimulates research into new areas of evolutionary biology.There are so many things I could ask. I'm tempted to ask the following question,
Many of us believe that the role of adaptation in evolutionary theory was considerably revised by the development of Neutral Theory and Nearly-Neutral Theory almost 50 years ago. These concepts, and the importance of random genetic drift, have been integrated into the standard textbooks for many decades. Why don't you ever talk about those challenges to the old 1940s version of the Modern Synthesis? Is it because you don't think they were significant additions to the old theory?
Friday, September 23, 2016
Random genetic drift is a process that alters allele frequencies within a population. The change is due to "random" events. It differs from natural selection where the change is due to selection for alleles that confer selective advantage on the reproductive success of an individual. Here's one description,
If a population is finite in size (as all populations are) and if a given pair of parents have only a small number of offspring, then even in the absence of all selective forces, the frequency of a gene will not be exactly reproduced in the next generation because of sampling error. If in a population of 1000 individuals the frequency of "a" is 0.5 in one generation, then it may by chance be 0.493 or 0.505 in the next generation because of the chance production of a few more or less progeny of each genotype. In the second generation, there is another sampling error based on the new gene frequency, so the frequency of "a" may go from 0.505 to 0.501 or back to 0.498. This process of random fluctuation continues generation after generation, with no force pushing the frequency back to its initial state because the population has no "genetic memory" of its state many generations ago. Each generation is an independent event. The final result of this random change in allele frequency is that the population eventually drifts to p=1 or p=0. After this point, no further change is possible; the population has become homozygous. A different population, isolated from the first, also undergoes this random genetic drift, but it may become homozygous for allele "A", whereas the first population has become homozygous for allele "a". As time goes on, isolated populations diverge from each other, each losing heterozygosity. The variation originally present within populations now appears as variation between populations.
Suzuki, D.T., Griffiths, A.J.F., Miller, J.H. and Lewontin, R.C.
in An Introduction to Genetic Analysis 4th ed. W.H. Freeman (1989 p.704)
A theology student named Derrick has written a review of Jerry Coyne's book Faith vs. Fact. He didn't like it very much. (Duh!) You can read his review at: Jerry Coyne, Faith Vs. Fact: Why Science and Religion Are Incompatible.Before reading that review, let's make sure we understand Jerry's position. Here's what he says on page xx of his book.
My main thesis is narrower and, I think, more defensible: understanding reality, in the sense of being able to use what we know to predict what we don't, is best achieved using the tools of science, and is never achieved using the methods of faith. That is attested by the acknowledged success of science in telling us everything from the smallest bits of matter to the origin of the universe itself—compared with the abject failure of religion to tell us anything about gods, including whether they exist.