Chris Nedin Enters the Blogosphere

 
Chris Nedin is an interrupted paleontologist who studied Ediacaran and Early Cambrian palaeontology, palaeoecology and taphonomy. He was one of the early regulars on the newsgroup talk.origins and he even came to a Howlerfest in Toronto a few years ago (1997).¹ (Chris lives in Australia.)

Chris Nedin has now become a blogger. Visit Ediacaran and read his first posting: The Spandrels of San Marco and the Anomalocaris Paradigm. Here's a teaser ..

The Spandrels of San Marco and the Panglossian Paradigm is one of my favourite science papers. As someone who accepts natural selection as a powerful evolutionary mechanism, but who considers that there are other, equally, or perhaps more, powerful mechanism out there, such as genetic drift, this paper resonated a lot with me. To summarise the paper (if you haven’t read it, please do), not everything that happens in evolution occurs because it was selected for. Like spandrels, things can happen as a consequence of other events. To summarise the summary, sh*t happens.

Here I’d like to develop that theme using Anomalocarus.

Welcome to the blogosphere, Chris. With an opening like that, we expect big things in the future.

---

1. I still remember how excited he and Saint Andrew (Andrew MacRae) were when the curators at the Royal Ontario Museum pulled out their famous fossil of Anomalocarus to look at. Chris and Andrew, being paleontologists, were the only ones allowed to touch it. Chris was also thrilled to see the trilobites with bite marks. Read his posting to see why.

What Does Marcus Antonius Tell Us about Evolution?

 
Meet my (probably mythical)¹ ancestor, Marcus Antonius (83 BC - 30 BC), better known as Mark Antony. (Color photo not available.)

Mark Antony was a friend, and cousin, of Gaius Julius Caesar, although after Caesar's assassination he stopped praising Caesar. Mark Antony had a falling out with Octavian (Augustus) after the Second Triumvirate split up and he ended up in Egypt. The history is kind of interesting but not very relevant.

We're mostly concerned about Mark Antony's genes. Near the end of his life he had three children by Cleopatra, Queen of Egypt; the twins Alexander Helios & Cleopatra Selene II and Ptolemy Philadelphus. This led to gene flow between the Italians and subpopulations in the Middle East. (There were other liaisons that contributed to gene flow in both directions between the Middle East and Europe.)

Before moving to Egypt, Mark had several wives in Rome. One of them was Octavia Major and they had a daughter, Antonia Minor. Antonia married Nero Claudius Drusus Germanicus and one of her sons was Claudius Cæsar (Tiberius Claudius Nero Germanicus), Emperor of Rome. At the time Antonia and Drusus were living in Lugdunum (Lyon, France).

Claudius married Valeria Messalina (granddaughter of Octavia) and their daughter was Genvissa (Venus Julia). Claudius then married Julia Agripina and had more children, including Emperor Nero. We aren't interested in Julia Agripina except to note her scientific contribution to the understanding of eukarotic transcription [Mushrooms for Dinner].

Genvisa married Arviragus, King of Siluria, in 45 AD. Siluria was a kingdom in the south of Wales and at the time they were resisting Roman occupation. Arviragus became King of the Britons. Their son was Meric (Marius) , King of the Britons. Do you see where this is headed?

Meric married Penardun and their son was Coel I "Old King", King of Siluria. Coel had a SON who in turn had an unnamed GRANDSON who had a daughter named Alofe (Aife).

Alofe married Fiachadh III Streabhruine, 120th Ard Righ of Ireland, and their son was Muirreadhach Tireach , King of Connought, 122nd Ard Righ of Ireland.

Muirreadhach married Murien and their son was Eochaidh Moihmeodhain (Echu Mugmedón), 124th Ard Righ of Ireland.

Eochaidh married Carthan Casduff and their son was Niall Nóigiallach - Niall of the Nine Hostages, my ancestor and the ancestor of about 100 million other people.

Thus, Marcus Antonius is also my ancestor.

The figure below show that the various subpopulations within Europe are genetically distinct (Novembre et al. 2008). See my recent posting, Genes and Geography with a link to Razib's explanation of the structure of populations at Gene Expression [Genetic map of Europe; genes vary as a function of distance].

This data represents only a small percentage of the genetic variation in Europeans. Much of the remaining variation does not show a geographic distribution like the one in the figure because the variants arose much earlier. They have had time to spread to all subpopulations, or perhaps they pre-date the founding of the European population.

Novembre et al. also had to restrict their analysis to those 1,387 individuals who had both sets of grandparents from the same region. Many of the remaining group of 1,805 individuals did not know where their grandparents were born but a substantial number had grandparents from two different regions. What this means is that there is substantial ongoing gene flow between the various subpopulations

What does this have to do with Mark Antony? Quite a bit, actually. Looking at the figure from the Nature paper one can't help but be struck by what it says about population structure and gene flow in the past. The pink individuals in the upper left-hand have clearly been partially isolated from the rest of the European population for quite some time—equivalent to about 40-60 generations.

We know that this group has received alleles from Italy via Mark Antony and Niall of the Nine Hostages and probably from a great many other Italians who were living in Roman Britain. This level of gene flow amounts to just a trickle and the foreign alleles might easily be diluted out by random genetic drift.

We can think of gene flow in the opposite direction by considering what might have happened if a favorable allele had arisen in the Irish population about 1500 years ago. While it might have spread rapidly in Ireland, chance are it would not have made much impression in the rest of the European subpopulations until very recently. All bets are off now that humans have become so mobile but it is worth keeping in mind that the populations of most other species probably look a lot like ours did only a few centuries ago.

New beneficial alleles will not make much headway in 2000 years because gene flow between subpopulations is very low. There's no reason to assume that it was any different in the ancient past—it may even have been worse. Think about that the next time you hear about some hypothetical allele that arose 50,000 years ago and became fixed in the entire species. That's not very likely.

---

1. See comments. It looks like Genvissa, the presumed daughter of Claudius, is a mythical character made up many centuries after her presumed marriage to the King of the Siluria.

Novembre J, Johnson T, Bryc K, Kutalik Z, Boyko AR, Auton A, Indap A, King KS, Bergmann S, Nelson MR, Stephens M, Bustamante CD (2008) Genes mirror geography within Europe. Nature, Published online 31 August 2008 [doi:10.1038/nature07331]

Niall Nóigiallach - Niall of the Nine Hostages

 
Niall Nóigiallach is a very famous man (Nóigiallach is Gaelic for "having Nine Hostages"). He was an Irish King who lived from about 350 to 405 AD. The "nine hostages" refers to hostages that he kept from each of the places that owed him allegiance.

Niall was fond of raiding the coast of Roman Britain and on one of those raids he captured a man named Maewyn Succat, who became a slave in Ireland. Succat eventually escaped, returned to Britain, and became a Christian missionary. He then went back to Ireland to convert the Irish heathens to Christianity. We know Maewyn Succat by his Christian name, Patrick, or Saint Patrick.

The reason Niall Nóigiallach is famous is because he is associated with the List of High Kings of Ireland, one of the oldest well-established genealogies in all of Europe. Anybody who connects to the lineage can trace ancestors back to about 100 AD.

Niall is also famous for another reason. DNA studies indicate that one in twelve Irish men carry a Y chromosome haplotype that traces back to Niall. The haplotype is also common in Scotland and England, and on the continent. This makes Niall one of only a handful of men who have millions of direct male descendants. (Genghis Khan was another [Genghis Khan a Prolific Lover, DNA Data Implies].)

Families that trace their ancestry back to Niall of the Nine Hostages include: (O')Neill, (O')Gallagher, (O')Boyle, (O')Doherty, O'Donnell, Connor, Cannon, Bradley, O'Reilly, Flynn, (Mc)Kee, Campbell, Devlin, Donnelly, Egan, Gormley, Hynes, McCaul, McGovern, McLoughlin, McManus, McMenamin, Molloy, O'Kane, O'Rourke and Quinn.

My mother's maiden name is Doherty. We are descendants of the O'Dochartaigh's of Donegal in the north-west part Ireland. Donegal is in the Republic of Ireland not in the part of Ulster that became what is now called "Northern Ireland", which is part of the United Kingdom. Donegal is near where the most intense spot on the DNA map is located.

My mother was hoping to establish the direct connection between her ancestors and the ancient lineage leading to Niall but it hasn't been possible. That was a big disappointment because I thought it would be fun to have a known ancestor from 400 AD.

Recently I discovered that my ancestors connect to the Niall lineage through English and through Scottish lines that are completely unrelated to the Doherty's. This shows, once again, that most people in England, Scotland, and Ireland are related if you go back far enough. The fact that so many lineages connect to the Niall lineage is not as significant as you might think. It's mostly because that ancient lineage is so well known.

In my case, the connections come through Isabel de Clare, grandmother of Robert the Bruce of Scotland, and through Isabel Mar, the wife of Robert the Bruce. Niall Nóigiallach is one of my ancestors.

If your ancestors are from the British Isles, chances are pretty high that we are related if we go back 60 generations. We all have about a trillion potential ancestors back then but that's five orders of magnitude more than all the people who lived in the British Isles at that time.

---

Happy Mole Day!

 
Today is "Mole Day," celebrated as part of National Chemistry Week. You can read all about it on Adventures in Ethics and Science [Happy Mole Day! (What's a mole?)].

What do you mean, "it's not that kind of mole?"¹

---

1. What would you call 6.02 × 10²³ Cindy Crawford moles?

Bar Graphs, Pie Charts, and Darwin

One of Ms. Sandwalk's ancestors is William Playfair (1789 - 1823). Her great grandfather—the great-great-grandfather of my children—was John Playfair Leslie. John's mother is a direct descendant of William Playfair.

William Playfair was an interesting man for many reasons. He is most famous for inventing statistical graphs; especially pie charts and bar graphs. These were printed in his famous book, Commercial and Political Atlas, published in 1786. Two examples of figures from that book are shown here.

But that's not all that Playfair did. His biographers call him an "engineer, political economist and scoundrel." I won't talk about the "scoundrel" part except to mention that it's probably an accurate description. One of the more legal things he did was to participate in the storming of the Bastille on July 14, 1789. (See William Playfair for some of the less legal activities.)

William Playfair was born in Scotland and lived with his older brother John Playfair in Edinburgh. John Playfair was a distinguished Professor of Mathematics at the University of Edinburgh. Their other brother was the architect James Playfair.

William Playfair was trained as an engineer with Andrew Meikle, the inventor of the threshing machine. Following his apprenticeship, he joined the company Boulton & Watt in Birmingham, England. This company operated a large plant that manufactured steam engines. William Playfair was assistant to James Watt.

It was during his time in Birmingham that Playfair made the connection that's so important to readers of Sandwalk.


In Birmingham, William Playfair associated with the members of the Lunar Society and attended their meetings. In addition to Matthew Boulton and James Watt, his bosses, there were other members whose names may be familiar; Josiah Wedgewood, Joseph Priestly, and Erasmus Darwin. Erasmus is Charles Darwin's grandfather. Josiah Wedgewood was Charles Darwin's other grandfather.

I keep hoping that one or more of my ancestors would have known Charles Darwin or even been related. No such luck. This is as close as it gets. My wife and children have an ancestor who hung out with Erasmus Darwin and Josiah Wedgewood.

I'm jealous.

---

Society Without God

 
From Amazon.com.

Before he began his recent travels, it seemed to Phil Zuckerman as if humans all over the globe were “getting religion” — praising deities, performing holy rites, and soberly defending the world from sin. But most residents of Denmark and Sweden, he found, don’t worship any god at all, don’t pray, and don’t give much credence to religious dogma of any kind. Instead of being bastions of sin and corruption, however, as the Christian Right has suggested a godless society would be, these countries are filled with residents who score at the very top of the “happiness index” and enjoy their healthy societies, which boast some of the lowest rates of violent crime in the world (along with some of the lowest levels of corruption), excellent educational systems, strong economies, well-supported arts, free health care, egalitarian social policies, outstanding bike paths, and great beer.

Zuckerman formally interviewed nearly 150 Danes and Swedes of all ages and educational backgrounds over the course of fourteen months, beginning in 2005. He was particularly interested in the worldviews of people who live their lives without religious orientation. How do they think about and cope with death? Are they worried about an afterlife? What he found is that nearly all of his interviewees live their lives without much fear of the Grim Reaper or worries about the hereafter. This led him to wonder how and why it is that certain societies are nonreligious in a world that seems to be marked by increasing religiosity. Drawing on prominent sociological theories and his own extensive research, Zuckerman ventures some interesting answers.

This fascinating approach directly counters the claims of outspoken, conservative American Christians who argue that a society without God would be hell on earth. It is crucial, Zuckerman believes, for Americans to know that “society without God is not only possible, but it can be quite civil and pleasant.”

”Most Americans are convinced that faith in God is the foundation of civil society. Society Without God reveals this to be nothing more than a well-subscribed, and strangely American, delusion. Even atheists living in the United States will be astonished to discover how unencumbered by religion most Danes and Swedes currently are. This glimpse of an alternate, secular reality is at once humbling and profoundly inspiring — and it comes not a moment too soon. Zuckerman’s research is truly indispensable.”
—Sam Harris

It's not just Denmark and Sweden. Many European countries are essentially secular as are many parts of Australia, New Zealand and Canada. Even in the USA, there are pockets of the country where the influence of religion is minimal.

Wake up Christians. Your religion is becoming increasingly superfluous. There's no point in being religious.

---

[Hat Tip: RichardDawkins.net]

Is Religion Here to Stay?

 
In the comments of a recent posting we heard the oft-repeated argument that a majority of Americans are believers and nothing is going to change that. It's an example of an irrational argument but it seems to be part of the defense mechanism of most believers.

I don't think it's true. I think the USA will change, just as Western Europe has changed. Here's what PZ Myers calls [A heartening graph].

There is one other possibility that some of my colleagues fear. Instead of a slow steady evolution away from superstition, we may see an ugly revolution in the USA as the two sides of the debate adopt mutually antagonistic points of view. There's an argument to be made that what many of us see as a hopeful sign is actually the precursor to establishment of a religous fundamentalist state—or at least a civil war where the attempt is made.

---

Happy Birthday Universe!

 
Bishop James Ussher (1581 - 1656) was Archbishop of Armagh and Primate of All Ireland. He calculated that the universe was created on this day in 4004 BC, or more correctly the night before this day.

In addition to astute Biblical scholarship, the calculation required a knowledge of ancient history. Ussher's estimates of ancient dates were pretty good for his time.

We now know that his calculation was flawed because the Bible is completely wrong about creation but it is unfair to make fun of Ussher based on what we learned several centuries later.

Happy Birthday Universe.

---

Nobel Laureate: Hermann Muller

 

The Nobel Prize in Physiology or Medicine 1946.

"for the discovery of the production of mutations by means of X-ray irradiation"

Hermann Joseph Muller (1890 - 1967) won the Noble Prize for showing that X-rays could induce mutations in Drosophila melanogaster. He was able to isolate and map specific mutations caused by X-rays showing that these were stable genetic changes.

For a brief description of the technique, see Hermann Muller Invented Balancer Chromosome.

The significance of Muller's work is described in the presentation speech on the Nobel rize website.

THEME:
Nobel Laureates

It was known, already at the turn of the century, that apparently sudden changes may appear spontaneously in the hereditary mass, which result in changes in the characteristics of the organism. We now know that these changes may be of different types, and among them occur also disturbances in individual genes. These are very rare, however. Even in such a convenient experimental object as the banana fly, introduced by Morgan, where the generations succeed each other rapidly, and thousands of flies can be examined, it is only seldom that mutations are observed. Muller grappled with the task of trying to change the frequency of mutations. He first created procedures, technically extremely elegant, by which the mutation frequency could be measured exactly. When this task - which took several years - had been completed, the effect of different agents on the frequency of mutations was investigated, and the discovery for which the Nobel Prize is now awarded was made, viz. that irradiation with X-rays evokes large numbers of mutations. Experiments could be arranged, for instance, so that nearly 100 per cent of the offspring of irradiated flies showed mutations. Thus a possibility had been created for the first time of influencing the hereditary mass itself artificially.

This discovery aroused a great sensation already when it was first published in 1927 and rapidly led to a great deal of work of different kinds and in the most varied directions. The mechanism of the effect of rays was studied by many research workers, with Muller at their head. Greatly simplified X-ray irradiation, as also ionizing irradiation, could be likened in general to a shower of infinitely small (even compared with the individual cell) but highly explosive grenades, which explode at different spots within the irradiated organism. The explosion itself (or the fragments it throws up) tears the structure of the cell to pieces or disturbs its arrangement. If such an explosion happens to take place in or close to a gene, its structure, and therewith also its effect on the organism, may be changed.

Muller's discovery of the induction of mutations by means of rays has been of tremendous importance for genetics and biology in general.

---

The Christian Man's Evolution

 
A posting on the Scientific American website describes the view of Francisco J. Ayala, a man who was ordained as a Dominican priest who is also an excellent scientist [The Christian Man's Evolution: How Darwinism and Faith Can Coexist .

Here's an excerpt ...

Ayala graduated in physics at the University of Madrid, then worked in a geneticist’s lab while studying theology at the Pontifical Faculty of San Esteban in Salamanca, Spain. By his ordination in 1960 he had already decided to pursue science instead of a ministerial role. At the monastery Darwinism had never been perceived as an enemy of Christian faith. So a year later, when Ayala moved to New York City to pursue a doctorate in genetics, the prevailing U.S. view of a natural hostility between evolution and religion was a shock.

Ever since, Ayala has attempted to address religious skepticism about Darwin’s theory. At first, he recalls, his scientific colleagues were wary and took the position that researchers should not engage in religious discussions. By 1981, when the Arkansas legislature voted to give creationism equal time in schools, the mood began to change. The National Academy of Sciences prepared an amicus curiae brief for a Supreme Court case on the Louisiana “Creation Act” and asked Ayala to lead the effort. The booklet became the 1984 Science and Creationism: A View from the National Academy of Sciences.

For the second edition in 1999 Ayala presented the idea of incorporating the words of some theologians but recalls, “I was almost eaten alive.” In the third edition, published this year, one section features statements by four religious denominations and three scientists on the compatibility of evolution with religious beliefs.

I've already commented on the National Academys' sellout to political correctness and on the fact that Ayala was Chair of the committee [Richard Dawkins on the Michael Reiss Affair] [National Academies: Science, Evolution and Creationism]. The fallacy here is something called The Doctrine of Joint Belief.

That's not what I want to comment on today. I want to draw your attention to the use of "Darwinism" in the title of the article and to "Darwin's theory" in the body of the article. The author, Sally Lehrman¹, should know better. If she's going to write for Scientific American then she better learn that the correct terms are "evolution" and "evolutionary theory." The editors of Scientific America should know better, but then what can you expect from a magazine that has fallen so far from its heydays in the 60s and 70s?

---

1. "Sally Lehrman teaches journalism in the public interest at Santa Clara University."

Hermann Muller Invented the Balancer Chromosome

Since writing about Balancer Chromosomes, I've gotten several email messages pointing out things I missed. Thanks to everyone who responded. It's what makes this blog worthwhile.

Quite a few readers pointed out that balancer chromosomes were invented a very long time ago by Hermann Muller. Muller won the Nobel Prize in 1946 for discovering mutagenesis by X-rays.

Dale Hoyt, a fly geneticist, sent me a description of Muller's experiment and he has given me permission to post it.

The first Nobel laureate who used balancers in his work was Hermann J. Muller. He used a strain of D. melanogaster that was heterozygous for an X-chromosome inversion. This suppresses crossing over between the normal X and the X carrying the inversion during meiosis. A single crossover within the inverted segment will generate a "bridge" at meiosis I, causing the non-crossover chromatid to preferentially segregate to the future ovum. In Muller's work the inverted X was marked with the dominant eye shape mutation, Bar, and carried a recessive lethal allele.¹ A female heterozygous for the marked inverted chromosome and a "wild type" chromosome will produce only 1/2 the normal number of male progeny and they will all be wild type. This is because 1/2 the males die because they receive the Bar chromosome and are hemizygous for the lethal. The inversion heterozygosity prevents recombination between the Bar locus and the lethal locus. Muller used this stock, called "ClB", to show that X-irradiation increased the frequency of mutation to lethal genes on the X-chromosome. Irradiated male flies were individually mated to the ClB females. Their Bar-eyed female offspring (heterozygous for the inversion and the irradiated X-chromosome) were mated to their brothers. If no males were produced from this cross then the irradiated male transmitted an X chromosome with a lethal mutation. It was easy to score the crosses—just look at the bottle and if there were no males then Muller knew that he had a radiation induced lethal.

---

1. l(1)C, associated with the left breakpoint of the inversions. Presumably the break disrupts a gene required for viability. The gene must be known by now.

[Photo Credit: WIRED]

The Lactose Paradox

The lac operon in E. coli consists of three genes (lacZ, lacY and lacA) transcribed from a single promoter. The lacZ gene encodes the enzyme β-galactosidase, an enzyme that cleaves β-galactosides. Lactose is a typical β-galactoside and the enzyme cleaves the disaccharide converting it to separate molecules of glucose and galactose. These monosacharides can enter into the metabolic pool of the cell where they can serve as the sole source of carbon.

LacY encodes a famous transporter called lactose permease. It is responsible for importing βgalactosides. The lacA gene encodes a transacetylase that is responsible for detoxifying the cell when it takes up poisonous β-galactosides.

[from The Lac Operon]

Transcription of the lac operon begins when RNA polymerase binds to the P_lac promoter. The long polycistronic mRNA (wavy line) is translated to produce the three proteins.

In the absence of lactose, transcription of the lac operon is blocked by a repressor protein that binds to two sites (O₁ and O₂) preventing RNA polymerase from transcribing the operon [Repression of the lac Operon].

When the bacteria encounter lactose, transcription of the lac operon is induced but since the operon has a weak promoter not much protein will be produced as long as glucose is present. Glucose is always the preferred carbon source. In the absence of both glucose and lactose the operon is maximally induced by the activator CRP-cAMP.

Lactose induces transcription by causing a change in the structure of the repressor so that it no longer binds to DNA. When that happens, RNA polymerase can transcribe the operon.

Here's the paradox. Lactose can't enter the cell unless it's transported across the membrane by the permease and the permease can only be made if the lac operon is transcribed. Furthermore, lactose itself doesn't bind to the lac repressor causing it to detatch from its binding sites. Instead, the actual inducer is allolactose, a modified form of lactose that can only be synthesized inside the cell by the enzyme β-galactosidase. β-galactosidase can only be synthesized if the operon is transcribed.

This is known as the "lactose paradox." It seems you can't induce the operon unless there's allolactose present and the only way to get allolactose is to take up lactose via the permease and convert it to allolactose via β-galactosidase.

The "paradox" was explained many decades ago when it was discovered that the lac operon is transcribed at least once whenever the lac repressor dissociates from its binding sites. The lac repressor is a highly specific DNA binding protein that binds very tightly to O₁ and O₂. But no protein can bind forever. When it dissociates, an mRNA is made and some permease and some β-galactosidase is synthesized. The repressor quickly re-binds and transcription is blocked.

The effect of this "escape" synthesis is that there will always be a few molecules of permease and a few molecules of β-galactosidase inside the cell. When the cell encounters lactose in the medium enough can be taken up and converted to allolactose to induce the operon.

A paper published in this week's issue of Science looked at the number of permease molecules that had to be present in order to induce transcription of the lac operon and discovered that there had to be about 300 molecules present. Some bacterial cells had fewer molecules of permease, by chance, so the repressor remained bound to DNA. Other cells had more than 300 molecules of permease so transcription of the operon was induced and many more molecules of permease were synthesized (Choi et al. 2008).

This is an interesting result but it might not be worth blogging about except for one thing. Our friendly IDiot DaveScot decided to use this paper to prove that evolution is wrong!! You can read all about it on Panda's Thumb: Scientific Vacuity of ID: Lactose Digestion in E. coli.

There's one more wrinkle to this story. Lactose is probably not the main substrate for β-galactosidase and it's quite likely that a typical E. coli cell never sees lactose. When they're not inside a human gut, E. coli cells won't ever encounter lactose. Even when they're living inside a friendly human, it will most often be an adult and throughout most of evolutionary history human adults did not consume milk. E. coli usually does not make up a significant proportion of the bacteria in nursing infants.

So, what is the real product of β-galactosidase and the real inducer of the lac operon? It's likely to be various other β-galactosides such as β-galactosyl glycerol. These are common breakdown products of plant membranes. They are transported efficiently by the permease but they can also be transported by a galactose permease that is always present in the bacteria membrane. Furthermore, β-galactosyl glycerol is a direct inducer of the lac operon. It binds directly to lac repressor so there's no need to convert it to something else (Egel, 1988).

While there may be a "lactose paradox" there is no "β-galactosyl glycerol paradox."

---

Choi, P.J., Cai, L., Frieda, K., and Xie, X.S. (2008) A stochastic single-molecule event triggers phenotype switching of a bacterial cell. Science 322:442-6. [DOI: 10.1126/science.1161427]

Egel, R. (1988) The "lac" operon: an irrelevant paradox? Trends in Genetics 4:31.

Adoptees use DNA to find surname

 
This is an example of a real ethical problem. You might be surprised to learn that there aren't all that many "real" ethical problems. Most of the ones that are proposed are pseudo-ethical problems.

In this case, an article from BBC News describe how Adoptees use DNA to find surname.

Male adoptees are using consumer DNA tests to predict the surnames carried by their biological fathers, the BBC has learned.

They are using the fact that men who share a surname sometimes have genetic likenesses too.

By searching DNA databases for other males with genetic markers matching their own, adoptees can check if these men also share a last name.

This can provide the likely surname of an adoptee's biological father.

Why is this an ethical problem? Because it (potentially) involves a conflict between the wishes of two individuals. The adoptee wants to know who his biological parents are and the biological parents may wish to remain unknown.

As far as I'm concerned, the wishes of the biological parents have to be respected but with the widespread use of commercial DNA testing services, this wish can be circumvented by a determined adoptee.

Incidentally, these tests are also going to reveal who isn't your father, and that's also a problem.

There are many blogs acting as cheerleaders for the new commercial DNA testing services. One of them, The Genetic Genealogist seems to think that finding out who your father is, or isn't, is a good thing. That blog even points to a commercial company runnnig a program for adoptees with a success rate of more than 30% [More On Revealing Surnames Using Genetic Genealogy].

I think it's about time we started to think about the consequences.

---

Gairdner Awards 2008

 
This is the week of the Gairdner awards. It's an excellent opportunity for undergraduates to see and hear some outstanding scientists. This week's lineup includes the 2008 winners and returning winners from past years.

Samuel Weiss: Adult neural stem cells
Victor Ambros: MicroRNA pathways in animal development
Gary Ruvkun: The tiny RNA pathways of C. elegans
Nahum Sonenberg: Translational control in biology and medicine
Harald zur Hausen: Infections as cancer risk factors
Ralph M. Steinman: Dendritic cells: A vehicle for vaccine development
Alan Bernstein: Progress towards an HIV vaccine
Sydney Brenner: An introduction
Craig Mello: RNAi from mechanism to medicine
Eric Olson: MicroRNa control of heart development and disease
George Church: Reading and writing genomes
Douglas Hanahan:Micro-RNA signatures in tumorigenesis
James S. Thomson: Exiting the pluripotent state, and back again
Gordon Keller: Directed differentiation of embryonic stem cells
Cynthia Kenyon: Genes and cells that regulate the lifespan of C. elegans
Leonard Guarente: Sirtuins, aging and diseases

The Gairdner Foundation presents a two-day symposium entitled "Minds That Matter" at the University of Toronto featuring academic lectures by Gairdner winners past and present, and other leading medical scientists. Attendance is open to anyone and is free of charge. All lectures are given at the Medical Sciences Auditorium on the University of Toronto campus in downtown Toronto.

TORONTO - UNIVERSITY OF TORONTO CAMPUS - MACLEOD AUDITORIUM
Date: Thursday, October 23, 2008

9:00 a.m.
Welcome: Dr. John Dirks, President, The Gairdner Foundation

Chair: Catharine Whiteside, Dean, Faculty of Medicine, Vice Provost Relations with Healthcare Institutions, University of Toronto

9:10 a.m.
Introduction: Dr. Freda Miller, Senior Scientist, Developmental & Stem Cell Biology, The Hospital for Sick Children, Professor, Department of Molecular Genetics, University of Toronto

Speaker: Dr. Samuel Weiss, Gairdner Laureate 2008, Professor of Cell Biology & Anatomy & Pharmacology & Therapeutics, Director Hotchkiss Brain Institute, University of Calgary, Calgary, AB, CA

Lecture: Adult neural stem cells: From basic science to therapeutic applications

9:50 a.m.
Introduction: Dr. Howard Lipshitz, Professor & Chair, Department of Molecular Genetics, Canada Research Chair (Tier 1) in Developmental Biology, University of Toronto, ON, CA

Speaker: Dr. Victor Ambros, Gairdner Laureate 2008, Professor of Molecular Medicine, University of Massachusetts Medical School, Worcester, MA, USA

Lecture: MicroRNA pathways in animal development

10:30 a.m.Break

10:45 a.m.
Introduction: Dr. Craig Smibert, Department of Biochemistry, University of Toronto

Speaker : Dr. Gary Ruvkun, Gairdner Laureate 2008, Department of Genetics, Harvard Medical School, Boston, MA, USA

Lecture: The tiny RNA pathways of C. elegans

11:25 a.m.
Introduction: Dr. Tony Pawson, University Professor, University of Toronto, Programme in Molecular Biology & Cancer, Samuel Lunenfeld Research Institute, Mount Sinai Hospital

Speaker: Dr. Nahum Sonenberg, Gairdner Laureate 2008, Professor, Department of Biochemistry and McGill Cancer Centre, McGill University, Montreal, Quebec, CA

Lecture: Translational control in biology and medicine

12:05 p.m. LUNCH

1:00 p.m.
Chair: Dr. Jack Gauldie, University Professor, Department of Pathology & Molecular Medicine, McMaster University, Director, Centre for Gene Therapeautics, Hamilton

1:05 p.m.
Introduction: Dr. Joan Murphy, Head of the Division of Gynecologic Oncology, UHN, Associate Professor, Department of Obstetrics & Gynecology, University of Toronto

1:10 p.m.
Speaker: Prof. Harald zur Hausen, Gairdner Laureate 2008, Deutsches Krebsforschungszentrum, Heidelberg, Germany

Lecture: Infections as cancer risk factors

1:40 p.m.
Introduction: Dr. Michael Julius, Vice President Research, Sunnybrook Health Sciences Centre, Toronto, CA

Speaker: Dr. Ralph M. Steinman, GairdnerLaureate 2003, Henry G. Kunkel Professor & Sr. Physician,The Rockefeller University, New York, NY, USA

Lecture: Dendritic cells: A vehicle for vaccine development

2:20 p.m.
Introduction: Dr. Janet Rossant, Chief of Research & Senior Scientist, Research Institute, The Hospital for Sick Children, Toronto, ON, CA

Speaker: Dr. Alan Bernstein, Gairdner Wightman Laureate 2008, Executive Director, Global HIV Vaccine Enterprise, New York, NY, USA

Lecture: Global solutions for global challenges: Progress towards an HIV vaccine

3:00 p.m. Dr. John Dirks
Conclusion

ADVANCES IN MOLECULAR BIOLOGY: MICRO RNA'S, STEM CELLS AND AGING

TORONTO - UNIVERSITY OF TORONTO CAMPUS - MACLEOD AUDITORIUM
Friday, October 24, 2008

9:00 a.m.
Welcome: Dr. John Dirks, President & Scientific Director, The Gairdner Foundation
Professor Paul Young, Vice President Research, University of Toronto, CA

Chair: Dr. Michael Hayden, Canada Research Chair in Human Genetics & Molecular Medicine, University of British Columbia, Vancouver, B. C.

Speaker: Dr. Sydney Brenner, Gairdner Laureate 1978 & 1991, Nobel Laureate 2002, Distinguished Professor, The Salk Institute, San Diego, CA, USA

Lecture: An introduction

9:30 a.m.
Introduction: Dr. Martin Simard, Laval University Cancer Research Centre, Quebec City, Montreal, CA

Speaker: Dr. Craig Mello, Nobel Laureate 2006, Gairdner Laureate 2005, Howard Hughes Medical Institute, University of Massachusetts Medical School, Worcester, MA, USA

Lecture: RNAi from mechanism to medicine

10:10 a.m. Break

10:30 a.m.
Introduction: Dr. David MacLennan, Gairdner Laureate 1991, Banting Best Department of Medical Research, University of Toronto, Charles H. Best Institute, Toronto, CA

Speaker: Dr. Eric Olson, Professor, Molecular Biology, Southwestern Medical School, Dallas, Texas

Lecture: MicroRNa control of heart development and disease

11:10 a.m.
Introduction: Dr. Steve Scherer, The Center for Applied Genomics, The Hospital for Sick Children, Toronto, CA

Speaker: Dr. George Church, Professor of Genetics, Harvard Medical School, Director of the Center for Computational Genetics, Boston, MA, USA

Lecture: Reading and writing genomes

11:50a.m. LUNCH

12:45 p.m.
Chair: Dr. Michael Tyers, CH Waddington Professor of Systems Biology, The University of Edinburgh, Edinburgh, ScotlandIntroduction: Dr. Samuel Aparicio, Professor of Breast Cancer Research, UBC/BCCA, BC Cancer Agency, Vancouver, BC

Speaker: Dr. Douglas Hanahan, Diabetes, and Comprehensive Cancer Centres, UCSF, San Francisco

Lecture: Micro-RNA signatures of the stages in multi-step tumorigenesis

1:25 p.m.
Introduction: Dr. Brenda Andrews, Terrence Donnelly Centre for Cellular & Biomolecular Research, University of Toronto, Toronto, CA

Speaker: Dr. James S. Thomson, Professor of Anatomy, University of Wisconsin Stem Cell & Regenerative Medicine Center, Wisconsin, USA

Lecture: Exiting the pluripotent state, and back again

2:05 p.m.
Introduction: Dr. Andras Nagy, Senior Investigator, Developmental Molecular Geneticist, Samuel Lunenfeld Research Institute, Mount Sinai Hospital, Toronto, CA

Speaker: Dr. Gordon Keller, Senior Scientist, Division of Stem Cell & Developmental Biology, Ontario Cancer Institute, Toronto, CA

Lecture: Directed differentiation of embryonic stem cells to functional tissues

2:45 p.m.
Introduction: Dr. Peter Lewis, Vice Dean, Research & International Relations, Faculty of Medicine, Professor of Biochemistry, University of Toronto, Toronto, CA

Speaker: Dr. Cynthia Kenyon, Director, Hillblom Center for Biology of Aging, UCSF, San Francisco, CA

Lecture: Genes and cells that regulate the lifespan of C. elegans

3:25 p.m.
Introduction: Dr. Jacques Drouin, Chair in Molecular Genetics, Intitut De Recherches Cliniques De Montreal, Montreal, Quebec

Speaker: Dr. Leonard Guarente, Harvard Medical School, Boston, MA, USA

Lecture : Sirtuins, aging and diseases

4:10 p.m.
Conclusion: Dr. John H. Dirks

---

Monday's Molecule #93

 
What's going on here? Your task is to identify the experiment that led to this result. It's a short step from there to this week's Nobel Laureate(s). You just need to switch species.

Here's a hint: This week's Nobel Laureate(s) and last week's Nobel Laureates have something in common.

You need to describe what you see in the figure as accurately as possible. Then identify the Nobel Laureate(s).

The first one to correctly identify the figure and name the Nobel Laureate(s), wins a free lunch at the Faculty Club. Previous winners are ineligible for one month from the time they first collected the prize. There are four ineligible candidates for this week's reward: Brad Hersh of Clemsen University, Alex Ling of the University of Toronto, Haruhiko Ishii, and Bill Chaney of the University of Nebraska.

THEME:

Nobel Laureates
Send your guess to Sandwalk (sandwalk (at) bioinfo.med.utoronto.ca) and I'll pick the first email message that correctly identifies the molecule and names the Nobel Laureate(s). Note that I'm not going to repeat Nobel Laureate(s) so you might want to check the list of previous Sandwalk postings by clicking on the link in the theme box.

Correct responses will be posted tomorrow. I reserve the right to select multiple winners if several people get it right.

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

UPDATE:The figure shows the result of an experiment where human cells in culture were irradiated with X-rays (Scherthan et al. 2008). There are two obvious chromosomal rearrangements. Breaks and deletions are common in X-ray treated cells. The Nobel Laureate is Hermann Muller who won the prize for creating mutants using X-rays. He worked with Drosophila melanogaster. Only one person got this one right and that person is ineligible.

---

[Figure Credit: The figure is from Scherthan et al. (2008)]

Scherthana, H., Hieberb, L., Braselmannb, H., Meinekea, V., and Zitzelsberger, H. (2008) Accumulation of DSBs in γ-H2AX domains fuel chromosomal aberrations. Biochemical and Biophysical Research Communications 371:694-697. [doi:10.1016/j.bbrc.2008.04.127]