Charles Darwin Was a Gradualist

 
Punctuated Equilibria refer to patterns of evolution characterized by long periods of stasis interrupted by shorter periods of evolutionary change. The changes are associated with speciation events where a new, changed, species splits off from the parental, unchanged, species. This is speciation by cladogenesis (splitting) as opposed to anagenesis, where a single species changes gradually into something different without splitting.

Stephen Jay Gould wrote a massive book on macroevolutionary theory that featured punctuated equilibria and its consequences such as species sorting. The original book was called The Structure of Evolutionary Theory. It's 1433 large pages long. Few people have read the entire thing. I am one.

Recently, the publishers of The Structure of Evolutionary Theory (Belknap Press of Harvard University Press) have brought out a new book by Stephen Jay Gould—a remarkable achievement since Gould died in 2002. As it turns out, the new book Punctuated Equilibrium, is just chapter nine of the large book; a 279 page chapter called Punctuated Equilibrium and the Validation of Macroevolutionary Theory. PZ Myers reviewed this book for New Scientist a few weeks ago [Punctuated Equilibrium by Stephen Jay Gould].

One of the significant impacts of Punctuated Equilibrium is the emphasis on episodic change rather than the gradualism that was so commonly believed to be the main pattern in evolution. Eldredge and Gould explain why gradualism was such a prominent part of evolutionary theory before punctuated equilibrium came along. Gould has extended that explanation in Structure and in numerous essays.

Gould points out that Charles Darwin was a firm believer in gradualism. Indeed, it was an essential component of Darwin's defense of evolution and his promotion of natural selection. Darwin's gradualism arose from his commitment to the uniformitarianism of Lyell and his emphasis on the vast age of the Earth. According to Gould there are several different meanings of gradualism but the one that conflicts with punctuated equilibria is the idea that change must be gradual at geological scales.

This is why Darwin said that nature does not proceed by leaps and it's why Darwin postulated that gaps in the fossil record were due to lack of data.

PZ Myers noted this in his review when he said,

Gould and Eldredge proposed punctuated equilibrium as a paleontologist's view of the history of life: they were describing the paleontological data available at the time pointing out that there was no geological evidence to support Charles Darwin's belief that species evolved gradually. Time has shown them to be correct, and their observations are now accepted by most biologists as a accurate account of evolutionary history.

Now, PZ is no dummy. He's been around the blogosphere and newsgroups long enough to know that calling Darwin a gradualist is like waving a red flag in front of a bull. There's a large group of Darwin apologists out there who will do anything to prove that Charles Darwin was right about everything, even if is has to be proved retrospectively (i.e., somehow we didn't notice that Darwin believed in punctuated equilibrium until 1972).

The first salvo was fired in the letters column in this week's issue of New Scientist. Wayne Bagguley writes,

I am shocked that someone as knowledgeable as P.Z. Myers is promoting the age-old myth about "Charles Darwin's belief that species evolved gradually" without periods of stasis. In On the Origin of Species Darwin wrote "Although each species must have passed through numerous transitional stages, it is probable that the periods, during which each underwent modifications, though many and long as measured by years, have been short in comparison with the periods which each remained in an unchanged condition. These causes, taken conjointly, will to a large extent explain why—though we do not find many links—we do not find interminable varieties connecting together all extinct and existing forms by the finest graduated steps."

Stephen Jay Gould is no dummy. As an expert on Darwin and the history of biology you can be sure that he's heard these complaints before. You can be certain that Gould has addressed them numerous times.

The longest, and best, defense of Darwin's gradualism can be found in chapter 2 of Structure. This is a 76 page chapter titled "The Essence of Darwinism and the Basis of Modern Orthodoxy." I'm sure PZ Myers has read this chapter and that's why he said what he said. Gould makes the point that,

SInce Darwin prevails as the patron saint of our profession, and since everyone wants such a preeminant authority on their side, a lamentable tradition has arisen for appropriating single Darwinian statements as defenses for particular views that either bear no relation to Darwin's own concerns, or that even confute the general tenor of his work.... I raise this point here because abuse of selective quotation has been particularly notable in discussion of Darwin's views on gradualism. Of course Darwin acknowledged great variation in rates of change, and even episodes of rapidity that might be labelled catastrophic (at least on a local scale); for how could such an excellent naturalist deny nature's multifariousness on such a key issue as the character of change itself? But these occasional statements do not make Darwin the godfather of punctuated equilibrium ....

You'll have to read Gould's chapter to see the case he makes because it's much too involved to summarize here. I do note one pithy comment to the effect that,

I will not play 'duelling quotations' with 'citation grazers,' though a full tabulation of relative frequencies could easily bury their claims under a mountain of statements.

He then proceeds to tabulate dozens of quotations that demonstrate Darwin's gradualism!

Natural Foods Contain Lots of "Carcinogens"

 
Bruce Ames was a Professor in the Department of Biochemistry & Molecular Biology at the University of California, Berkeley (USA). This is one of the leading departments of biochemistry in the entire world. Bruce Ames is currently a senior scientist at the Children's Hospital Oakland Research Institute (CHORI) in Oakland, California (USA).

Ames developed the Ames test, a biological test to detect chemicals that are mutagenic. He has published dozens of papers on mutagens and mutagenesis and dozens of papers on human health and nutrition.

The Ames test is used to create a database of possible cancer-causing chemicals. One of the important issues is the question of where these potential carcinogens can be found. Is it only synthetic compounds that pose a danger? Is it true that "natural" products are much safer? This is the issue that John Tierney raises in his New York Times article [see Did Rachel Carson Get It Right?]. Tierney elaborates on his website where he refers to the work of Bruce Ames [see Synthetic v. Natural Pesticides].

The answer is pretty clear, even though it is not widely appreciated. There are plenty of chemicals in natural products that test positive in the Ames test and test positive in tests for cancer using rodents. Since we eat far more natural products that synthetic products, it follows that we are far more likely to get cancer from eating "healthy" foods than from eating at a fast food restaurant.

Here's the abstract from a classic paper by Ames and Lois Swirsky Gold from 1998.

The idea that synthetic chemicals such as DDT are major contributors to human cancer has been inspired, in part, by Rachel Carson's passionate book, Silent Spring. This chapter discusses evidence showing why this is not true. We also review research on the causes of cancer, and show why much cancer is preventable. Epidemiological evidence indicates several factors likely to have a major effect on reducing rates of cancer: reduction of smoking, increased consumption of fruits and vegetables, and control of infections. Other factors are avoidance of intense sun exposure, increases in physical activity, and reduction of alcohol consumption and possibly red meat. Already, risks of many forms of cancer can be reduced and the potential for further reductions is great. If lung cancer (which is primarily due to smoking) is excluded, cancer death rates are decreasing in the United States for all other cancers combined. Pollution appears to account for less than 1% of human cancer; yet public concern and resource allocation for chemical pollution are very high, in good part because of the use of animal cancer tests in cancer risk assessment. Animal cancer tests, which are done at the maximum tolerated dose (MTD), are being misinterpreted to mean that low doses of synthetic chemicals and industrial pollutants are relevant to human cancer. About half of the chemicals tested, whether synthetic or natural, are carcinogenic to rodents at these high doses. A plausible explanation for the high frequency of positive results is that testing at the MTD frequently can cause chronic cell killing and consequent cell replacement, a risk factor for cancer that can be limited to high doses. Ignoring this greatly exaggerates risks. Scientists must determine mechanisms of carcinogenesis for each substance and revise acceptable dose levels as understanding advances. The vast bulk of chemicals ingested by humans is natural. For example, 99.99% of the pesticides we eat are naturally present in plants to ward off insects and other predators. Half of these natural pesticides tested at the MTD are rodent carcinogens. Reducing exposure to the 0.01% that are synthetic will not reduce cancer rates. On the contrary, although fruits and vegetables contain a wide variety of naturally-occurring chemicals that are rodent carcinogens, inadequate consumption of fruits and vegetables doubles the human cancer risk for most types of cancer. Making them more expensive by reducing synthetic pesticide use will increase cancer. Humans also ingest large numbers of natural chemicals from cooking food. Over a thousand chemicals have been reported in roasted coffee: more than half of those tested (19/28) are rodent carcinogens. There are more rodent carcinogens in a single cup of coffee than potentially carcinogenic pesticide residues in the average American diet in a year, and there are still a thousand chemicals left to test in roasted coffee. This does not mean that coffee is dangerous but rather that animal cancer tests and worst-case risk assessment, build in enormous safety factors and should not be considered true risks. The reason humans can eat the tremendous variety of natural chemical "rodent carcinogens" is that humans, like other animals, are extremely well protected by many general defense enzymes, most of which are inducible (i.e., whenever a defense enzyme is in use, more of it is made). Since the defense enzymes are equally effective against natural and synthetic chemicals one does not expect, nor does one find, a general difference between synthetic and natural chemicals in ability to cause cancer in high-dose rodent tests. The idea that there is an epidemic of human cancer caused by synthetic industrial chemicals is false. In addition, there is a steady rise in life expectancy in the developed countries. Linear extrapolation from the maximum tolerated dose in rodents to low level exposure in humans has led to grossly exaggerated mortality forecasts.

Ames, B.N. and Gold, L.S. (1998) The causes and prevention of cancer: the role of environment. Biotherapy 11:205-20.

Did Rachel Carson Get It Right?

 
Rachel Carson is widely credited with kick starting the environmentalist movement following publication of Silent Spring back in 1962. She pointed out the dangers of widespread use of DDT and promoted the idea that synthetic chemicals can cause cancer.

Many scientists take issue with the "facts" in her book and they believe that she may have done more harm than good. If you care about scientific accuracy then you must be skeptical about her claims, even if you admire her goals.

Carson was born on May 27, 1907 and last month marked the 100th anniversary of her birth.

For a summary of where she went wrong you might as well start with a recent New York Times article by John Tierney [Fateful Voice of a Generation Still Drowns Out Real Science]. Tierney outlines the case very well and he has attracted a lot of attention by not pulling his punches.

For Rachel Carson admirers, it has not been a silent spring. They’ve been celebrating the centennial of her birthday with paeans to her saintliness. A new generation is reading her book in school — and mostly learning the wrong lesson from it.

This is the kind of science journalism that I admire but, as you might imagine, Tierney has come under fierce attack from those people who value superstition over rationalism. Tierney has attempted to deal with those attacks on his website [Synthetic v. Natural Pesticides].

There are many issues here but one of the most interesting is whether the essence of Carson's claim is accurate. Is it true that a large percentage of cancers is caused by synthetic chemicals in the environment? That certainly seems to be the general perception both inside and outside the scientific community.

Does this controversy remind you of the framing debate? It's clear that Rachel Carson used very effective framing in advocating her opposition to chemicals in the environment. The metaphor of a "Silent Spring" being only one of many examples. At the time there may have been many scientists who agreed with her about the dangers of DDT and, by extension, many other synthetic chemicals.

However, it's clear that there were also scientists who disagreed, as John Tierney points out in his New York Times piece. The problem is that once scientists start down the framing pathway they open a Pandora's Box that's very hard to close. I think that scientists have to be very, very, careful about abandoning objectivity and skepticism in order to push a political agenda. Once they jump on the bandwagon it's very hard to jump off if the scientific evidence fails to support the agenda. And that hurts the credibility of science.

Militant Atheists

 
Have you ever wondered why so many atheists are described as "militant" atheists? Read why on Jeff Shallit's blog Recursivity [Why Are Atheists Always Described as Militant?].

D-Day

 

Today marks the 63rd anniversary of the invasion of Normandy on June 6, 1944. British, Canadian and American forces opened the second front against Germany.

For baby boomers it means a day of special significance for our parents. In my case, it was my father who took part in the invasions. He was an RAF pilot flying rocket firing typhoons in close support of the ground troops. During the initial days his missions were limited to quick strikes and reconnaissance since Normandy was at the limits of their range from southern England. During the second week of the invasion his squadron landed in Normandy and things became very hectic from then on with several close support missions every day.

The photograph shows a crew loading rockets onto a typhoon based just behind the landing beaches in Normandy.

Today's D-Day is very different. It's the day when Leslie (Ms. Sandwalk) and I are meeting with the people involved in my daughter's wedding on June 29th at the University of Toronto Faculty Club. This is the day when we have to lock in many of the decisions; such as flowers, cakes, music, and number of guests. Very scary.

Don't for one minute think that I have much of a role here. I'm just along for the ride. Leslie and Jane are in charge.

Nobel Laureates: Aaron Ciechanover, Avram Hershko, Irwin Rose

 
The Nobel Prize in Chemistry 2004.

"for the discovery of ubiquitin-mediated protein degradation"



Aaron Ciechanover (1947- ), Avram Hershko (1937- ) and Irwin Rose (1926- ) won the Nobel Prize in 2004 for discovering the mechanism of ubiquitin mediated protein degradation [Protein Turnover]. You can view an animation of this process on the Nobel Prize website. It's called Kiss of Death.

The presentation speech was delivered by Professor Lars Thelander of the Royal Swedish Academy of Sciences on December 10, 2004. Note that the individual contributions of the three winners are not specified. They worked together on many of the problems associated with the mechanism. You can read their individual acceptance speeches to see how they present their own work.

Your Majesties, Your Royal Highnesses, Ladies and Gentlemen,

This year's Laureates in Chemistry are being rewarded for their discovery of life's own death-labeling system and at the same time for having solved a scientific mystery.

The cells in our bodies contain about one hundred thousand different proteins. Proteins do all the work in the cell, and proteins are directly responsible for its shape and function. One of the things proteins do is to build up the molecular machines that form our muscles; another is to form the enzymes that accelerate and control the various chemical reactions that are necessary for life.

Now, how can a cell possibly keep track of all its proteins? Protein molecules are synthesized and broken down all the time at a high rate. As to the synthesis of proteins, we have a good understanding of how this is regulated at molecular level, and the research here has been rewarded with a number of Nobel Prizes. In contrast, the break down of proteins in the cell has been considered less interesting, and it has attracted few researchers.

This year's Laureates in Chemistry, Aaron Ciechanover, Avram Hershko and Irwin Rose, went against the stream. They studied precisely how the breakdown of proteins is regulated in the cell. What aroused their interest was reports in the literature that the breaking down of proteins inside living cells requires energy. This seemed a paradox since everybody knew that, for example, the degradation of proteins in the intestines – that is, outside the cell – takes place with no requirement for added energy. Why is energy needed for degradation inside cells?

By studying the mechanisms of energy-dependent protein degradation in cell extracts, this year's three Laureates succeeded at the beginning of the 1980s in identifying a completely new principle for protein degradation. They discovered a system that used a type of "death label" together with three different enzymes to attach it to the proteins to be destroyed. The energy goes to activating the label and enabling the cell to control the process accurately.

The death label itself is a small protein called ubiquitin. The name comes from the Latin ubique, which means 'everywhere' and tells us that the protein is found in the cells of almost all organisms. Among all the proteins in the cell, the enzyme system chooses a certain unwanted protein molecule and tags it with the death label. The labeled protein molecule is transported to a type of waste disposer inside the cell called the proteasome, which recognizes the label rather like a key fitting into a lock. Before the labeled protein is sucked into the waste disposer for destruction, the label is removed so that it can be used again to death label more proteins. Inside the waste disposer, the doomed protein is chopped to pieces. These can later be used for synthesizing new proteins. It was first believed that controlled protein degradation is used only to destroy faulty proteins, which may otherwise damage the cell. Prion diseases and Alzheimer's disease represent similar cases. Yet constantly growing research has shown something more: that it is at least as important for the cell, by destroying a protein with a certain function, to be able to regulate a biochemical reaction, rather like when you turn off a switch. We now know that controlled protein degradation regulates other very important processes in the cell as well. Examples are the cell cycle, repair of DNA damage and immune defense. In plants, the process is also needed to prevent self-pollination. And a failure in our degradation system may lead to disease.

The discovery of controlled protein degradation explains, at molecular level, the function of a regulation system that is very central for the cell. Among other things, the knowledge can be used to produce new medicines against different diseases.

Professor Ciechanover, Professor Hershko, Dr. Rose,
Your discovery of a system for controlled protein degradation in cells has fundamentally changed our way of thinking about protein degradation. We can now understand at molecular level how the cell controls a number of central biochemical processes. More reactions regulated by ubiquitin-mediated protein degradation are being identified every year. On behalf of the Royal Swedish Academy of Sciences, I wish to convey to you our warmest congratulations, and I now ask you to step forward to receive the Nobel Prize in Chemistry from the hands of His Majesty the King.

SCIENCE Questions: What Determines Species Diversity?

 
"What Determines Species Diversity?" is one of the top 25 questions from the 125th anniversary issue of Science magazine [Science, July 1, 2005]. The complete reference is ...

Pennisi, Elizabeth (2005) What Determines Species Diversity? Science 309: 90. [Text] [PDF]

Elizabeth Pennisi is a news writer for Science magazine. She has been publishing articles there for at least ten years. She had previously written about genes and genomes, including earlier articles about the number of genes in the human genome and one of the other top 25 Science questions [Why Do Humans Have So Few Genes?]

The question is poorly phrased because it's really about speciation.

Understanding what shapes diversity will require a major interdisciplinary effort, involving paleontological interpretation, field studies, laboratory experimentation, genomic comparisons, and effective statistical analyses. A few exhaustive inventories, such as the United Nations' Millennium Project and an around-the-world assessment of genes from marine microbes, should improve baseline data, but they will barely scratch the surface. Models that predict when one species will split into two will help. And an emerging discipline called evo-devo is probing how genes involved in development contribute to evolution. Together, these efforts will go a long way toward clarifying the history of life.

Paleontologists have already made headway in tracking the expansion and contraction of the ranges of various organisms over the millennia. They are finding that geographic distribution plays a key role in speciation. Future studies should continue to reveal large-scale patterns of distribution and perhaps shed more light on the origins of mass extinctions and the effects of these catastrophes on the evolution of new species.

This question is also related to a more fundamental question; namely, what is a species?

This certainly counts as one of the top questions in biology. If we ask it in the form "What causes speciation?" then it gets us into a discussion about punctuated equilibria, founder effects and all kinds of other controversial problems. It also brings up the issue of the role of natural selection and environment in speciation. While there may not be anything new to discover, there are many open questions concerning the mechanisms of speciation. Does sympatric speciation happen, for example?

There are many who think that natural selection plays only a minor role in most speciation events and there are many who think that environmental change is not correlated with speciation [Adaptation and Accident in PNAS, Evolution of Mammals].

Protein Turnover

 
One might assume that only growing or reproducing cells would require new protein molecules—and therefore a supply of amino acids—but this is not the case. Proteins are continually synthesized and degraded in all cells, a process called turnover. Individual proteins turn over at different rates. Their half-lives can vary from a few minutes to several weeks but the half-life of a given protein in different organs and species is generally similar. Rapid protein turnover ensures that some regulatory proteins are degraded so that the cell can respond to constantly changing conditions. Such proteins have evolved to be relatively unstable. The rate of hydrolysis of a protein can be inversely related to the stability of its tertiary structure—misfolded and unfolded proteins are quickly degraded.

In eukaryotic cells, some proteins are degraded to amino acids in the lysosomes. In these cases, vesicles containing material to be destroyed fuse with lysosomes, and various lysosomal proteases hydrolyze the engulfed proteins. The lysosomal enzymes have broad substrate specificities, so all the trapped proteins are extensively degraded.

Some proteins have very short half-lives because they are specifically targeted for degradation. Abnormal proteins are also selectively hydrolyzed. The pathway for the selective hydrolysis of these proteins in eukaryotic cells requires the protein ubiquitin. Ubiquitin is Monday's Molecule #29. It is a small, highly conserved protein of about 76 amino acid residues.

Side-chain amino groups of lysine residues in the target protein are covalently linked to the C-terminus of ubiquitin in a complex pathway that involves ubiquitin-activating enzyme (E1), ubiquitin-conjugating enzyme (E2), and ubiquitin-protein ligase (E3). This pathway is coupled to ATP hydrolysis—one ATP molecule is hydroylzed for every ubiquitin molecule attached to the target protein. The ubiquitinated protein is hydrolyzed to peptides by the action of a large multiprotein complex called the proteasome (or proteosome). This process occurs in both the cytosol and the nucleus.

Other proteases catalyze hydrolysis of the resulting peptides. ATP is required to assemble the proteasome and to hydrolyze the ubiquitinated protein. Before this pathway was discovered there was no explanation for the surprising observation that the degradation of many proteins requires ATP.


Adapted from Horton et al. Principles of Biochemistry 4th edition
©Laurence A. Moran and Pearson/Prentice Hall

SCIENCE Questions: How Does a Single Somatic Cell Become a Whole Plant?

 
"How Does a Single Somatic Cell Become a Whole Plant?" is one of the top 25 questions from the 125th anniversary issue of Science magazine [Science, July 1, 2005]. The complete reference is ...

Vogel, Gretchen (2005) How Does a Single Somatic Cell Become a Whole Plant? 309: 86.
[Text] [PDF]

Gretchen Vogel is a contributing correspondent for Science magazine. She is based in Berlin.

This question is really about developmental biology. It's closely related to the two questions that immediately precedes it in the journal: How Can a Skin Cell Become a Nerve Cell?, and What Controls Organ Regeneration?. For some reason the editors of Science seem to think that there's a fundamental difference between this question and the other two. Perhaps they think that plants control gene expression by a very different process?

The totipotency of plant cells was demonstrated half a century ago as noted in the article.

Nearly 50 years ago, scientists learned that they could coax carrot cells to undergo such embryogenesis in the lab. Since then, people have used so-called somatic embryogenesis to propagate dozens of species, including coffee, magnolias, mangos, and roses. A Canadian company has planted entire forests of fir trees that started life in tissue culture. But like researchers who clone animals (see p. 85), plant scientists understand little about what actually controls the process. The search for answers might shed light on how cells' fates become fixed during development, and how plants manage to retain such flexibility.

I really don't think it's correct to say that "plant scientists understand little about what actually controls the process." Furthermore, even if there are lots of details to be worked out, I see no indication that there's some mysterious unknown process behind plant development.

This is not a fundamental question.

bio::blogs #11

 
The 11th edition of bio::blogs, a carnival on bioinformatics, has been published at nodalpoint.org [Bio::Blogs #11].

A special edition of highlights can be found at Bioinformatics Zen [Bio::blogs 11 - special edition].

Did Dinosaurs Have Feathers?

 
An article on the National Geographic website addresses an issue in the evolution of birds ["Feathered" Dinosaur Was Bald, Not Bird Ancestor, Controversial Study Says].

The article deals with a recent report by a group at the University of KwaZulu-Natal in South Africa; University of North Carolina (Chapel Hill); and the Chinese Academy of Sciences, in Beijing. The paper was published in the journal Proceedings of the Royal Society B. The authors claim that the "feathers" seen on recent dinosaur fossils are not feathers at all but collagen fibers. This is a minority opinion and the reason why I mention the article is to point out how good science writing can put things in context. Here's an example,

Lingham-Soliar and colleagues' results support the arguments of a small but highly vocal group of scientists who say there's no evidence of dinosaurs ever having feathers.

"The existence of protofeathers in these dinosaurs was considered critical evidence that birds were derived from dinosaurs," said study co-author Alan Feduccia, a bird evolution expert at the University of North Carolina at Chapel Hill.

"What we have shown is that there's absolutely no evidence whatsoever that protofeathers existed in dinosaurs, period."

But the majority of scientists in the field are unconvinced.

The article then goes on to quote from a number of scientists who disagree with the findings of the South African group.

"These people have been flogging the same horse for a long time," said Kevin Padian, curator of the University of California Museum of Paleontology.

"It is appalling that Proceedings B chose to publish this nonsense."

We need more of this kind of reporting.

Lingham-Soliar, T., Feduccia, A., and Wang, X. (2007) A new Chinese specimen indicates that ‘protofeathers’ in the Early Cretaceous theropod dinosaur Sinosauropteryx are degraded collagen fibres. Proc. Roy. Soc. B: published online Wednesday, May 23, 2007

Monday's Molecule #29

 

Today's molecule is my first example of a protein. I've given you two different views of the molecule showing most of it as a ribbon model. A small stretch of the polypeptide is displayed as a stick model. You have enough information to identify the protein provided you have taken the appropriate courses in high school or college. All we need is the name of the protein but if you can identify the species and the PDB file that would be an impressive feat of detective work.

As usual, there's a connection between Monday's molecule and this Wednesday's Nobel Laureate(s). This one is an direct connection. Once you have identified the molecule the Nobel Laureate(s) are obvious.

The reward (free lunch) goes to the person who correctly identifies both the molecule and the Nobel Laureate(s). Previous free lunch winners are ineligible for one month from the time they first collected the prize. There are no ineligible candidates for this Wednesday's reward since recent winners have declined the prize on the grounds that they live in another country and can't make it for lunch on Thursday. There was no winner last week although several people were close.

Comments will be blocked for 24 hours. Comments are now open.

Mendel's Garden #15

 
Visit The Daily Transcript for your complete list of summer reading, courtesy of Gregor Mendel Mendel's Garden #15 - Summer Reading Edition]. Of course you'll already know about what causes wrinkled peas because you've been reading Sandwalk. Don't let that put you off. There's plenty of other good stuff there.

Take the Carnegie Mellon University Survey on Ethical Standards

 
This is a survey on ethics developed by workers at Carnegie Mellon University for readers of the New York Times [Survey on Ethical Standards]. We can take the survey thanks to John Tierney and his blog TierneyLab: Putting Ideas in Science to the Test [Test Your Ethics (or Lack Thereof)].

The nice thing about this survey is that you can instantly see how you answered the questions relative to everyone else who took the survey. I was very pleasantly surprised at some of the responses. If you take the survey, make sure you do it alone and in a private place. You must answer all questions honestly and you may not want friends or relatives to know your answers. Try it, and then see how everyone else answered the questions.

I've been trying to stimulate some discussion about ethics without much success [Ethical Issues in Biochemistry]. There's a growing tendency in science education to include classes on ethics but nobody seems to be able to define ethics in a way that makes sense to me. What, exactly, is an ethical issue? [see, Ethics on Wikipedia] Take the survey to see if your sense of "ethics" agrees with others.

The other problem is how do you teach ethics to undergraduate science students? What are the basic principles of ethical reasoning? Is ethical relativism a valid philosophy or are there some "rules" that every undergraduate should memorize? [see, Moral Relativism on Wikipedia] I've encountered scientists who claim that we need to teach students that ethical relativism is a failed philosophy and there really is a "right" and a "wrong."

Here's a question that's not on the survey. Does whether or not you would have your genome sequenced [Sequencing Jim Watson] count as an ethical question? I don't think so. It's a question about personal preferences and the answer depends very much on how you feel personally about issues such as privacy. This isn't "ethics" as far as I'm concerned.

Sequencing Jim Watson

 
Jim Watson has just become the first person to have his complete genome sequenced. Craig Venter's genome sequence is not far behind.

Watson's genome was sequenced at the Baylor College of Medicine's sequencing center in collaboration with 454 Life Sciences, a private company that developed some new sequencing techniques. Apparently, the sequence was completed in two months at a cost of $1,000,000. Watson received the results on two DVDs. He promises to deposit it in the public database except for the sequence of his apolipoprotein E gene. He does not want to know which allele he carries because some of them are associated with Alzeimer's disease.

Here's the question for the day. Would you want to know the sequence of your genome if all you had to do was supply a small blood sample to get it? What are the implications? Do your children have a say if you intend to release your genome sequence into the public domain.

I can tell you that I would not do it. Perhaps the older I get the more I'm inclined not to care which alleles I carry but I would always be concerned about what effect it might have on my children—although that may be an unrealistic concern since they seem to have gotten all their good genes from me!

Watson is 79 years old and has two grown children.

[Genome of DNA discoverer is deciphered]
[Nobel Laureate James Watson Receives Personal Genome]
[Project Jim, celebrity sequencing, and the divine right of geneticists]