Debating philosophers: The difference between genes and alleles

This is my third post on the Lu and Bourrat (2017) paper [Debating philosophers: The Lu and Bourrat paper]. Part of their argument is to establish that modern evolutionary theory is a gene-centric theory. They need to make this connection because they are about to re-define the word "gene" in order to accommodate epigenetics.

In my last post I referred to their defense of the Modern Synthesis and quoted them as saying that the major tenets of the Modern Synthesis (MS) are still the basis of modern evolutionary theory. They go on to say,

Debating philosophers: The Modern Synthesis

I'm discussing a paper by Lu and Bourrat (2017) [Debating philosophers: The Lu and Bourrat paper]. They begin by describing current evolutionary theory, known (to them) as the Modern Synthesis. The paper is about challenges to current evolutionary theory from those who advocate an extended evolutionary synthesis or from those who would replace, rather than extend, current evolutionary theory. It is reasonable to begin with a description of the theory that's being challenged.

Here's what Lu & Bourrat say,

Debating philosophers: The Lu and Bourrat paper

John Wilkins posted a link on Facebook to a recent paper by his colleagues in Australia. The authors are Qiaoying Lu of the Department of Philosophy at Macquarie University in Sidney Australia and Pierrick Bourat of the Department of Philosophy at The University of Sydney in Sidney Australia.

Lu, Q., and Bourrat, P. (2017) The evolutionary gene and the extended evolutionary synthesis. The British Journal for the Philosophy of Science, (advanced article) April 20, 2017. [doi: 10.1093/bjps/axw035] [PhilSci Archive]

Abstract: Advocates of an ‘extended evolutionary synthesis’ have claimed that standard evolutionary theory fails to accommodate epigenetic inheritance. The opponents of the extended synthesis argue that the evidence for epigenetic inheritance causing adaptive evolution in nature is insufficient. We suggest that the ambiguity surrounding the conception of the gene represents a background semantic issue in the debate. Starting from Haig’s gene-selectionist framework and Griffiths and Neumann-Held’s notion of the evolutionary gene, we define senses of ‘gene’, ‘environment’, and ‘phenotype’ in a way that makes them consistent with gene-centric evolutionary theory. We argue that the evolutionary gene, when being materialized, need not be restricted to nucleic acids but can encompass other heritable units such as epialleles. If the evolutionary gene is understood more broadly, and the notions of environment and phenotype are defined accordingly, current evolutionary theory does not require a major conceptual change in order to incorporate the mechanisms of epigenetic inheritance.

1 Introduction
2 The Gene-centric Evolutionary Theory and the ‘Evolutionary Gene’
      2.1 The evolutionary gene
      2.2 Genes, phenotypes, and environments
3 Epigenetic Inheritance and the Gene-Centred Framework
      3.1 Treating the gene as the sole heritable material?
      3.2 Epigenetics and phenotypic plasticity
4 Conclusion

The selfish gene vs the lucky allele

The Selfish Gene was published forty-one years ago (1976) and last year there was a bit of a celebration. I think we can all appreciate the impact that the book had at the time but I'm not sure it's as profound and lasting as most people believe ["The Selfish Gene" turns 40] [The "selfish gene" is not a good metaphor to describe evolution] [Die, selfish gene, die!].

The main criticisms fall into two categories: (1) the primary unit of selection is the individual organism, not the gene, and (2) the book placed too much emphasis on adaptation (Darwinism). I think modern evolutionary theory is based on 21st century population genetics and that view puts a great deal of emphasis on the power of random genetic drift. The evolution of a population involves the survival of individuals within the population and that, in turn, depends on the variation that exists in the population. Thus, evolution is characterized by changes in the frequencies of alleles in a population.

Professor, please can I have more marks?

I submitted my grades on Thursday morning and they were approved by the Department of Biochemistry in short order. Once the final grades have been approved and submitted to the Faculty they can't be changed unless the change is approved by the Departmental Chair. Students may appeal their grade by paying a fee to re-read their final exam but, even then, I do not have the authority on my own to change a grade. I have to justify any change in writing. This is a good thing.

A few hours after the grades were posted I received an email message from a student [It's that time of year, again]. Here's part of what the student said,

I just saw my final mark ... which was an 76, and was very surprised. I thought I'd done well on the final exam, and had studied hard. My performance on the Midterm was good, and I had expected this to be just as well. As such, I wanted to humbly inquire whether it'd be possible to move me a 77 (a 1% increase) or even an 80. This small difference could make a very big impact on my GPA as I apply for positions to pursue a master or other professional degrees. With the mark as it is now, I fall below the GPA requirement for a program I wish to enroll in next year and will have to do another few courses or a full year to make up for it.

I'm going to Chicago!

I leave tomorrow for Chicago where I'm attending Experimental Biology 2017. Is anyone else going to be there? Wanna get together? I'm there until Wednesday.

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Bill Martin is coming to town!!!

Contact me by email if you'd like to meet him on Sunday, April 30th.

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The last molecular evolution exam: Question #6

How can alleles be fixed in a population by positive natural selection (i.e. adaptation) if the environment remains constant for thousands of years?

Question #1, Question #2, Question #3, Question #4, Question #5, Question #6

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The last molecular evolution exam: Question #5

Many people believe that recombination evolved because it increases genetic variation in a population and this provided a selective advantage over species that didn’t have recombination. Do you agree with this explanation for the evolution of recombination? Why, or why not? What are the other possibilities?

Question #1, Question #2, Question #3, Question #4, Question #5, Question #6

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The last molecular evolution exam: Question #4

More than 90% of our genome is transcribed when you add up all the transcripts from various cell types and various times of development (= pervasive transcription). Many biologists take this as evidence that most of the DNA in our genome is functional. What are the counter-arguments? Who do you believe and why?

Question #1, Question #2, Question #3, Question #4, Question #5, Question #6

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The last molecular evolution exam: Question #3

The Three Domain Hypothesis has eukaryotes and archaea branching off from eubacteria. It shows eukaryotes more closely related to archaea than to eubacteria. However, many scientific studies indicate that a majority of our genes are more similar to eubacterial genes than to archaeal genes. How do you explain this apparent conflict?

Question #1, Question #2, Question #3, Question #4, Question #5, Question #6

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The last molecular evolution exam: Question #2

The paper by Andrews et al. (2011) lists a number of common misconceptions held by their students. One of them is the idea that, “Evolution is a process that will never stop, even in the human species.” Why do they think this is a misconception? Do you agree?

Andrews, T.M., Kalinowski, S.T., and Leonard, M.J. (2011). “Are humans evolving?” A classroom discussion to change student misconceptions regarding natural selection. Evolution: Education and Outreach, 4:456-466. [doi: 10.1007/s12052-011-0343-4]

Question #1, Question #2, Question #3, Question #4, Question #5, Question #6

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The last molecular evolution exam: Question #1

Eugene Koonin described his view of the proper null hypothesis for evolutionary questions. One of the examples he used concerns the evolution of recent gene duplications (Koonin, 2016 p.5). Describe how one possible fate of these genes relates to constructive neutral evolution. What are the other possible fates of these genes? Which one is most likely?

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]

... in eukaryotes, duplicates of individual genes cannot be effectively eliminated by selection and thus often persist and diverge. The typical result is subfunctionalization, whereby the gene duplicates undergo differential mutational deterioration, losing subsets of ancestral functions. As a result, the evolving organisms become locked into maintaining the pair of paralogs. Subfunctionalization underlies a more general phenomenon, denoted constructive neutral evolution (CNE).

Question #1, Question #2, Question #3, Question #4, Question #5, Question #6

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Vimy Ridge

Today marks the 100th anniversary of the beginning of the Battle of Vimy Ridge. The battle invovled four divisions of the Canadian Corps and it has become a symbol for Canada of the sacrifices made during World War I. The symbol is remarkable for the beautiful Canadian National Vimy Ridge Memorial designed by Walter Seymour Allward. He intended it to be a "sermon against the futility of war."

It is remarkably successful as such a symbol since, among other things, it contains the names of more than 11,000 Canadians who died in World War I and whose bodies were never recovered. We visited the memorial in 2011 with my granddaughter Zoë [Canadian National Vimy Memorial] and found the name of Lance Corporal Robert Alexander Hood, a cousin of Leslie's grandfather and Zoë's great-great-grandfather.

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Somatic cell mutation rate in humans

A few years ago, Tomasetti and Vogelstein (2015) published a paper where they noted a correlation between rates of cancer and the number of cell divisions. They concluded that a lot of cancers could be attributed to bad luck. This conclusion didn't sit well with most people for two reasons. (1) There are many well-known environmental effects that increase cancer rates (e.g. smoking, radiation), and (2) there's a widespread belief that you can significantly reduce your chances of getting cancer by "healthy living" (whatever that is). The first objection is based on solid scientific evidence but the second one is not as scientific.

Some of the objections to the original Tomasetti and Vogelstein paper were based on the mathematical models they used to reach their conclusions. The authors have now followed up on their original study with more data. The paper appears in the March 24, 2017 issue of Science (Tomasetti and Vogelstein, 2017). If you're interested in the debate over "bad luck" you should read the accompanying review by Nowak and Waclaw (2017). They conclude that the math is sound and many cancer-causing mutations are, in fact, due to chance mutations in somatic cells. They point out something that should be obvious but bears repeating.