Why does the human population carry an allele that increases the risk of Alzheimer's?

The human apolipoprotein E gene (ApoE) has several alleles segregating in the human population. One of them, E4, is associated with increased risk of Alzheimer's. Ed Yong, writing for The Atlantic, asks "Why Do Humans Still Have a Gene That Increases the Risk of Alzheimer's?

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.”

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The pervasive transcription controversy: 2002

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.

Pyruvate dehydrogenase astonishes Ann Gauger

Ann Gauger was reading a cell paper the other day [Digging Deep in Biology: "Things Get Even More Complicated When You Look Closer"]. The subject was the localization of citric acid cycle enzymes and pyruvate dehydrogenase (PDH). She did a little digging and this is what astonished her ...

... 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.

Why are most biologists adaptationists?

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.

The dynamic duo tell us about five problems with evolution

Here's a link to a remarkable radio interview with Stephen Meyer and Doug Axe. The subject is the Royal Society meeting last November on New trends in evolutionary biology: biological, philosophical and social science perspectives. The theme is not Intelligent Design Creationism, instead it's all about so-called problems with evolutionary theory. That's really what ID is all about in spite of what the IDiots may claim. [see A Royal Pain: Stephen Meyer and Douglas Axe on Five Problems for Evolution.]

Here are the five problems according to IDiots.

1. Fossil record (Cambrian explosion)
2. The origin of information (no known natural source of information)
3. The necessity of early mutations (you can't mutate regulatory genes that act early in development because all mutations in those genes are lethal)
4. Epigenetic information (you can't evolve new body plans by mutating DNA because development is controlled by non-DNA epigenetic information)
5. The universal design intuition that we all have (everybody thinks that people are created by a god-like designer, even atheists, so it must be true)

What the heck is epigenetics?

"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].

Genetic variation in the human population

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.")

Birth and death of genes in a hybrid frog genome

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.

Do seahorses evolve faster?

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

Save the date!!! Michael Lynch is coming to Toronto

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.

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The exit exam for biochemistry and molecular biology students

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?

You MUST read this paper if you are interested in evolution

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.

The Edge question 2017

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 most popular Sandwalk post of 2016

My most popular post last year was: An Intelligent Design Creationist disputes the evolution of citrate utilization in the LTEE ... Lenski responds. It had almost 20,000 views and 227 comments.

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.

Intelligent Design Creationists reveal their top story of 2016

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?

Creationists list the top ten stories of 2016

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 ...

Is the high frequency of blood type O in native Americans due to random genetic drift?

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.

Nature opposes misinformation (pot, kettle, black)

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.

The ENCODE publicity campaign of 2007

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.

The proteome complexity myth

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.

Revisiting Michael Behe's challenge and revealing a closed mind

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 best countries for atheists

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!

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.

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Using conservation to determine whether splice variants are functional

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.

Restarting the function wars (The Function Wars Part V)

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).

How many proteins in the human proteome?

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.

Suzan Mazur doesn't like Carl Zimmer

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."]

Kevin Laland's new view of evolution

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.

Learning about modern evolutionary theory: the drift-barrier hypothesis

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.

On explaining science to the general public

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,

Edinburgh, Scotland

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.

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Extending evolutionary theory? - Melinda Zeder

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.

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