Otangelo Grasso is a creationist who's convinced he can learn to understand biochemistry by reading what's on the internet and copy-pasting it into his website. He then takes that limited knowledge and concludes that evolution is impossible. He often poses "gotcha" questions based on his flawed understanding.
His behavior isn't very different from most other creationists who suffer from Dunning-Kruger Disease but he happens to be someone who I thought could be educated.
I was wrong.
Over the years I've tried to correct a number of errors he's made so we could have an intelligent discussion about evolution. You can't have such a discussion if one side ignores facts and refuses to learn. Here's an example of a previous attempt: Fun and games with Otangelo Grasso about photosynthesis. Here's a post from yesterday showing that I wasted my time: Otangelo Grasso on photosynthesi.
Photosynthesis is the series of reactions that capture light energy and use it to make ATP and sometimes reducing equivalents (e.g NADPH). There are many different versions of photosynthesis. One of the simplest is found in purple bacteria where the process results in formation of a proton gradient that's used to drive ATP synthesis.
I just realized that I don't have a post devoted to the evolution of the citric acid cycle. This need to be remedied since I often talk about it. It's a good example of how an apparently irreducibly complex pathway can arise by evolution. It's also a good example to get students to think outside of the box. Undergraduate biochemistry courses usually concentrate on human physiology and too often students transfer that bias to all other species. They assume that what happens in humans is what happens in plants, fungi, protozoa, and bacteria.1
Here's what the standard citric acid cycle looks like (Moran et al., 2011 p. 393).
This is so frustrating. I've been debating creationists for almost 30 years. My colleagues and I have tried time and time again over those three decades to educate them about real evolutionary theory. We've also tried to teach them about the difference between evolution and the history of life. In order to explain the history of life on Earth you need to account for mass extinctions and other chance events that have nothing to do with evolution. They refuse to listen.
The theory of evolution by natural selection operating on random mutations, as a sweeping explanation for life and how it got there, is a "narrative." It presents a very smooth story, persuasive to most scientists. The facts may all be true, but the conclusion: BS.
No knowledgeable scientist thinks that natural selection is the only mechanism of evolution so no knowledgeable scientist thinks that mutation + selection explains the history of life. That's just BS. Not only are scientists aware of what modern evolutionary theory actually says but they're also aware of other factors that determined the history of life.
Now you know why we call them IDiots. What is it that makes them so resistant to learning about the ideas they so adamantly oppose? They can still oppose correct ideas if they want. Isn't that better than fighting strawmen?
I can think of several answers off the top of my head. The most important one is that Alzheimer's has very little effect on your ability to have children. The disease may not even have developed in most of our ancestors who tended to die younger. In order to be subject to negative selection the allele has to affect adults before they reproduce.
The second reason is that the slight deleterious effect, if there is one from an evolution perspective, may not have been significant enough in small populations. I know, and I hope my students know, that neutral and deleterious alleles can reach significant frequency in a population by chance. The general public doesn't know this.
Check out Ed Yong's article to see his explanation.
“It doesn’t make sense,” says Ben Trumble, from Arizona State University. “You’d have thought that natural selection would have weeded out ApoE4 a long time ago. The fact that we have it at all is a little bizarre.”
I'm working on a chapter about pervasive transcription and how it relates to the junk DNA debate. I found a short review in Nature from 2002 so I decided to see how much progress we've made in the past 15 years.
Most of our genome is transcribed at some time or another in some tissue. That's a fact we've known about since the late 1960s (King and Jukes, 1969). We didn't know it back then, but it turns out that a lot of that transcription is introns. In fact, the observation of abundant transcription led to the discovery of introns. We have about 20,000 protein-coding genes and the average gene is 37.2 kb in length. Thus, the total amount of the genome devoted to these genes is about 23%. That's the amount that's transcribed to produce primary transcripts and mRNA. There are about 5000 noncoding genes that contribute another 2% so genes occupy about 25% of our genome.
... so I looked up pyruvate dehydrogenase and found to my astonishment that it is not one enzyme but an enormous complex of three different enzymatic activities clustered together on a cube-shaped core of 24 units, or alternatively a dodecahedral core of 60 units. The enzymes work together to turn pyruvate into acetyl CoA in a three-step process, handing off to each other as the reaction proceeds.
I enjoyed listening to Michael Lynch's talk on Friday. Much of what he said has been covered in Sandwalk over the past few years. His main point was that nothing in biology makes sense except in the light of population genetics. He laments the fact that most biologists, and even most evolutionary biologists, don't have a firm grasp of population genetics and the importance of random genetic drift.
I asked him why he thought this was true. He said he didn't know why. I think he was being polite. If you read his book, "The Origins of Genome Architecture," you'll see that he attributes this phenomeon to ignorance of modern evolutionary theory.
"Epigenetics" is the (relatively) new buzzword. Old-fashioned genetics is boring so if you want to convince people (and grant agencies) that you're on the frontlines of research you have to say you're working on epigenetics. Even better, you can tell them that you are on the verge of overthrowing Darwinism and bringing back Jean-Baptiste Lamarck.
But you need to be careful if you adopt this strategy. Don't let anyone pin you down by defining "epigenetics." It's best to leave it as ambiguous as possible so you can adopt the Humpty-Dumpty strategy.1 Sarah C.P. Williams made that mistake a few years ago and incurred the wrath of Mark Ptashne [Core Misconcept: Epigenetics].
With a current population size of over 7 billion, the human population should contain a huge amount of genetic variation. Most of it resides in junk DNA so it's of little consequence. We would like to know more about the amount of variation in functional regions of the genome because it tells us something about population genetics and evolutionary theory.
A recent paper in Nature (Aug. 2016) looked at a large dataset of 60,706 individuals. They sequenced the protein-coding regions of all these people to see what kind of variation existed (Lek et al., 2016) (ExAC). The group included representatives from all parts of the world although it was heavily weighted toward Europeans. The authors used a procedure called "principal component analysis" (PCA) to cluster the individuals according to their genetic characteristics. The analysis led to the typical clustering by "population clusters." (That term is used to avoid the words "race" and/or "subspecies.")
De novo genes1 are quite rare but genome duplications are quite common. Sometimes the duplicated regions contain genes so the new genome contains two copies of a gene that was formerly present in only one copy. "Common" in this sense means on a scale of millions of years. Michael Lynch and his colleague have calculated that the rate of fixed gene duplication is about 0.01 per gene per million years (Lynch and Conery, 2003 a,b; Lynch 2007). Since a typical vertebrate has more than 20,000 genes, this means that 200 genes will be duplicated and fixed every million years.
The initial duplication event is likely to be deleterious since there will now be redundant DNA in the genome. The slightly deleterious allele (duplication) can be purged by negative selection in species with large population sizes (e.g. bacteria). But in species with smaller populations, natural selection is not powerful enough to eliminate slightly deleterious alleles so the duplication persists and may become fixed in the population.
Genome sequencing is becoming so routine that it's difficult to publish your new genome sequence in a top journal. The trick is to find something unique and exciting about your genome so you can attract the attention of the leading journals. The latest success is the seahorse genome published in the Dec. 15, 2016 issue of Nature (Lin et al., 2016.
The species is the tiger tail seahorse Hippocampus comes. The assembled genome is 502Mb or about 1/6th the size of the human genome. The seahorse has 23,458 genes (protein-coding?) or about the same number as most other vertebrates. About 25% of the genome is junk (transposon-related).1
Michael Lynch is giving a seminar next week on Friday, January 13, 2017 in the Dept. of Ecology and Evolutionary Biology at the University of Toronto. The title is: Mutation, Drift, and the Origin of Subcellular Features. The talk is at 3PM in the Earth Sciences Centre rm B142.
I'm a big fan of teaching fundamental concepts and principles and a big fan of teaching critical thinking. I think the most effective way of accomplishing these objectives is some form of student-centered learning. As I near the end of my teaching career, I wonder how we can tell if we succeed? It should be relatively easy to develop an exit exam for our biochemistry/molecular biology students to see if they grasp the basic concepts and can demonstrate an ability to think critically.
Here are some of the questions we could have on that exam. Each one requires a short answer with an explanation. The explanation doesn't have to be detailed or full of facts, just the basic idea. Students are graded on their ability to think critically about the answers. Many of the questions don't have a simple answer. Can you think of any other questions?
A reader alerted me to a paper that was just published in BMC Biology.1 The author is Eugene Koonin. He makes the case for neutral evolution (random genetic drift) and against adaptationism. You may not agree with his take on evolutionary theory but you better be aware of it if you claim to be knowledgeable about evolution.
Koonin, E.V. (2016) Splendor and misery of adaptation, or the importance of neutral null for understanding evolution. BMC biology, 14:114. [doi: 10.1186/s12915-016-0338-2]
The study of any biological features, including genomic sequences, typically revolves around the question: what is this for? However, population genetic theory, combined with the data of comparative genomics, clearly indicates that such a “pan-adaptationist” approach is a fallacy. The proper question is: how has this sequence evolved? And the proper null hypothesis posits that it is a result of neutral evolution: that is, it survives by sheer chance provided that it is not deleterious enough to be efficiently purged by purifying selection. To claim adaptation, the neutral null has to be falsified. The adaptationist fallacy can be costly, inducing biologists to relentlessly seek function where there is none.
Every year John Brockman asks his stable of friends an interesting question. Brockman is a literary agent and most of the people who respond are clients of his. (I want to be one.) The question and responses are posted on his website Edge. This year's question is, "What scientific term or concept ought to be more widely known?"
This year, the introduction is more interesting than the responses. Here's part of what Brokman wrote,
The article discussed a paper by Intelligent Design Creationist Scott Minnich who criticized Richard Lenski's ongoing evolution experiment on the grounds that no new information had been created in the evolution of ability to use citrate.
Yesterday I posted an article on: Creationists list the top ten stories of 2016 . Some of you may have noticed that there were only nine stories. That's because Evolution News & Views didn't post their top story until today. I was pretty sure what it would be.
Let me remind you of the main point I made yesterday. Intelligent Design Creationists claim to have scientific evidence of intelligent design. They claim their movement is focused on demonstrating intelligent design but not on proving anything about who the designer might be.
But that's not what the movement is all about. Most of their writings and speeches are focused on attacking evolution. They hope that by discrediting evolution and science they will, by default, support the case for gods (false dichotomy). They also hope that by promoting gaps in our knowledge they will lend support to those who want to insert gods into the gaps.
You don't need to take my word for it. Just look at what they think are the top stories of 2016. Most of their top nine stories were critiques of science in one way or another. There wasn't a single top story that advanced the case for intelligent design.
So, what about the #1 story? Is it going to be different?
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 ...
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.
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 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'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 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.
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.
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.
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.
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).
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.
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]:
Black = Grave Violations
Red = Severe Discrimination
Orange = Systemic Discrimination
Yellow = Mostly Satisfactory
Green = Free and Equal
Gray = No Rating
Here's the result for the entire world.
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!
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.
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.
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."
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.
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."]
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.
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.1979.0086
I 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.
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…
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?
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,
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.
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.
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.
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.
Susan Antón is a professor of anthropology at New York University (New York, NY, USA).
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.
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?
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."
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.
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.
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.
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?
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.
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.
At some point this flagrant misrepresentation of facts must be stopped. It's hurting science.
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.
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.
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.
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 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.
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.
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’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.
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'm not going to ask any questions after this talk. I'll report back on how many people seem to agree with him.
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.
