Death to Apostates?

 
There was a conference in the UK where a number of former adherents of Islam talked about the fact that rejecting Islam is a very serious offense. Apostates can be killed.

A.C. Graying wrote an article about the conference. It was published in The Guardian and you can read it on RichardDawkins.net.

Now Nesrine Malik has responded in Friday's issue of The Guardian [Death for apostasy?].

Here's part of what she says ...

As a Muslim who has lived most of my life in Muslim countries, this picture is hard to recognise. I have several friends and family members who are non-believers and apart from some efforts to return them to the straight and narrow or at least go through the motions of religious observance, they have not come into any physical danger. A close friend – hitherto religious – only recently sent me a long, tortured email detailing his journey away from Islam and from all religion; he expressed no fears for his life or safety, merely trepidation at the prospect of acclimatising to this new God-free world view.

Although the Council of Ex-Muslims and AC Grayling depict the threat to life and limb as an indisputable fact, in reality there are differences of opinion among Muslim scholars (ostensibly the hard core of the religion) regarding the death penalty for apostates.

This is not to say that Muslim governments – and Arab ones in particular – have a tolerant view of apostasy but the death threat is invoked only rarely and more for political reasons rather than religion ones: to set an example or to save face as a proxy punishment for challenging the social or political status quo. While this is in no way acceptable, it is an extension of the general lack of enshrined civic human rights and evolved political institutions and processes – a historical, social and geo-political reality in many Muslim countries that makes a mockery of any comparison to the experience of those renouncing Christianity or Judaism.

It's of little comfort to an ex-Muslim to learn that there is disagreement within the Muslim community about whether they should be put to death or not. They take only a little more comfort from the fact that the death penalty is only used "rarely."

I admire Nesrine Malik for stating that killing apostates is "in no way acceptable" but she weakens her case a great deal by making excuses. Just because killing apostates is part of a larger intolerant viewpoint is an explanation, but not an excuse. Personally, I don't much care how the members of a cultural group run their lives but I draw the line when they interfere with others. People who leave the group are making a choice and they should be left alone.

Malik claims that many ex-Muslims try to make themselves into martyrs by claiming they have been threatened with death. They are just using "the emotive power of 'death for apostasy' to serve their own ends, be they personal or political." That may or may not be true—it probably is—but that's not the point.

The point is that outspoken Muslims like Nesrine Malik should make their opposition to 'death for apostasy' much clearer than just throwing away a phrase like "no way acceptable" to be immediately followed with a reason why it's understandable.

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The Toronto Star Editorial Cartoon

 
Today's editorial cartoon in The Toronto Star is worth sharing. If Canadians were allowed to vote in the US Presidential elections, the McCain people would have waved the white flag months ago.

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The Toronto Star Opposes PR, Again

 
I don't get it. Why are the editors of The Toronto Star against proportional representation? Their reasoning doesn't make sense.

Last year the editorial board opposed the Ontario referendum on electoral reform. Their arguments were so stupid and factually incorrect that "Public Editor" Kathy English was obliged to defend the newspaper's editorial opinions [The Toronto Star Defends Its Editorial Policy on MMP].

She didn't do a very good job.

Today The Star has an editorial opposing any proportional electoral system. The paper notes that a nationwide proportional system of voting would have given a different distribution of seats than the result of last Tuesday's election. They note that the Green party would have probably gotten a number of seats.

The editorial states, correctly, that we can't just recalculate the results based on Tuesday's voting because if we had voted under a proportional system people wold have voted differently. They say ...

Furthermore, the analysis is backward looking – transposing last week's results onto a new system. In all likelihood, if Canada had a system of proportional representation, the outcome would be very different, given the demographical and geographical diversity of the country. The pro-life Christian Heritage Party, for example, might win enough votes to get seats. And new parties might emerge to win seats – say, an Alberta First party or even ethnic parties.

So Harper might be kept in power by entering a coalition with pro-life and Alberta First parties. Now that, indeed, is a scary prospect.

This is scary. It looks like the editors of The Star are afraid of proportional voting because (horrors!) some people might elect MP's who truly represent their points of view.

Now we certainly can't have that in a democracy, can we?

The scare tactics are not based on rational analysis of what happens in other countries. Most Western democracies have moved into the 21st century and they find it beneficial to let the people have their say. Sticking with an unfair first-past-the -post system only breeds disillusionment and bitterness with a system that disenfranchises a majority of voters. (Voter turnout on Tuesday dropped below 60%.)

It's time for The Toronto Star to find new editors—ones who are as progressive as the newspaper they work for. The current editors are clearly not up to the job.

But maybe we shouldn't expect too much from editors who put Madonna on the front page under a banner about a rape probe.

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Barack Obama Is my Cousin!

 
George Bush and I share a common ancestor. This isn't as surprising as it might seem. Just about anyone in North America who has relatives from the British Isles will be able to trace some of their ancestors back five or six hundred years if they dig hard enough.

There's an excellent chance that you can connect at some point to several well-known lineages, usually those involving kings and queens. In my case I eventually hook up with Mary Stewart (1380 - 1458) who is the daughter of Robert III, King of Scotland. She married George Douglas (1376 - 1402).

George Bush descends from Mary's sister Elizabeth Stewart who married James Douglas, brother of George Douglas [The Ancestry of George Bush].¹

Now, most of you might not be too excited about being related to George Bush but here's the good news ... I'm also related to Barack Obama according to Obama and Bush related.

That's pretty cool. It explains a lot.

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1. It's possible that Bush descends from Beatrice Sinclair and not Elizabeth Stewart—the website is confusing. Even if this is an error there are several other connections.

If you build it, will they follow?

I'm going to subject you to one of my pet peeves.

The University of Toronto is in the process of replacing all its pathways. I really like the new style of path even though it's probably very expensive. It will improve the look of the university.

That's not the peeve. Look at the photograph below. It shows the newly completed paths leading up from the subway stop on the corner of University and College (behind me). The ramp is the easiest access to my building. Several hundred people a day walk up the path from the subway stop and up the ramp into the building.

When the stone masons were building the path I mentioned that the old pathway didn't align with the much newer ramp and, consequently, people were cutting across the grass in order to save time. That's why the grass is worn away at the base of the ramp. The guys who were laying the stones agreed that the fancy new path should at least clip off the corner by the lamp post to encourage people to follow it.

They were overruled by their supervisor who claims he doesn't have the authority to move or change the paths. So they simply replaced the old paved pathway with the nice new stone blocks and moved on.

How ridiculous. My pet peeve is this. You should build pathways where people actually walk and not where you want them to walk.

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What Questions about Evolution Can Students Safely Ask?

 
Denyse O'Leary is upset about the fact that students who challenge evolution may be perceived as being unworthy [Intelligent design and popular culture: What questions about evolution can students safely ask?].

She was impressed with the suggestions made by some photographer so she reproduced them on her blog. Here's what Densye O'Leary thinks will stump the average Professor. This is just for amusement on a Friday afternoon.

Don't argue against him. Agree with him. Then ask a question like one of those below:

1. I’d like to shut up those stupid IDers once and for all. Please tell me where I can find a book that shows clearly all the transitional fossil forms between fish and amphibians or reptiles and birds or some such major transition. I’d like to see it spelled out in detail with pictures and measurements and explanations of each fossil so I can crush those idiots.

2. I know that evolution is the most solidly proven theory in all of science, so please show me the mathematical proof of how random changes create information. I’m sure there must be one because this is a fundamental truth of evolution.

3. I know that in any system like life on earth that is open and receives outside energy the system will steadily grow more and more complex but I don’t really understand the physics of this. Could you explain it to me?

Just in case you've forgotten, this is what passes as the best evidence for Intelligent Design Creationism. We should think up a name to describe these people.

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Jonathan Wells reviews the Christiane Nüsslein-Volhard and Wieschaus Experiment

In his book, Icons of evolution, Jonathan Wells has ten chapters devoted to refuting evolution. This is typical behavior for an Intelligent Design Creationist. There's no mention anywhere in the book of positive evidence for intelligent design.

One of the chapters is "Four-Winged Fruit Flies." The main point of the chapter is that most of the Drosophila developmental mutations are lethal or extremely deleterious so they can't be transitional states in evolution. Yet, according to Wells, the textbooks are full of misleading statements claiming that morphological mutations supply the raw material for evolution. Wells says that there's no evidence for any beneficial mutations in spite of the fact that they have been looked for.

Yet the evidence cited in these textbooks falls far short of supporting those sweeping claims. To be sure, biochemical mutations lead to antibiotic and insecticide resistance, and human beings carrying the sickle-cell trait are more likely to survive malaria as infants. But only beneficial morphological mutations can provide the raw materials for morphological evolution, and evidence for such mutations is surprisingly thin. As we have seen, four-winged fruit flies do not provide the missing evidence, despite their current popularity.

If textbook-writers have no good examples of beneficial morphological mutations, it's not because biologists haven't been looking for them About the time that Lewis was studying Ultrabithorax, German geneticists Christiane Nüsslein-Volhard and Eric Wieschaus were using a technique called "saturation mutagenesis" to search for every possible mutation involved in fruit fly development. They discovered dozens of mutations that affect development at various stages and produce a variety of malformations. Their Herculean efforts earned them a Nobel prize (which they shared with Lewis), but they did not turn up a single morphological mutations that would benefit a fly in the wild. [my emphasis]

The experiment that was performed by Christiane Nüsslein-Volhard and Eric Wieschaus was designed to detect recessive lethal mutations that affected development. These kind of mutations are likely to identify genes that are essential for development. I described the experiment in a separate posting [Balancer Chromosomes].

Note that the experiment was specifically designed to detect deleterious mutations—lethal being about as deleterious as you can get. It could not possibly have detected beneficial mutations, as Wells claims, since these would have been discarded early on when the mutant lines were established.

Was the true purpose of the experiment a well-kept secret known only to insiders? Hardly. Everyone who read the papers knew that the screen was for recessive lethals. In her Nobel lecture Christiane Nüsslein-Volhard says,

In 1979, Eric Wieschaus and I, at that time in the EMBL, Heidelberg, had developed the methods for the large scale screening for embryonic lethal mutations in Drosophila. The screening procedure focused on the segmented pattern of the larval epidermis (8). In this and subsequent screens, a number of new genes acting in the embryo and required for the formation of a morphologically normal larva were discovered (9-11).

Should Wells have known this? You be the judge.

Wells has a Ph.D. in biology, molecular and cell biology, from the University of California, Berkeley (USA). He worked on embryology and evolution as a graduate student and subsequently as a post-doctoral fellow in the laboratory of Carolyn Larabell at Berkeley. He published two papers on development in 1996 and 1997.

It's safe to assume that Wells understands the basic principles of genetics and developmental biology.

Could Wells have misunderstood the purpose of the Nüsslein-Volhard & Wieschaus experiment? No, Wells may be an IDiot but he's not that stupid. When Wells makes an issue of the fact that Nüsslein-Volhard & Wieschaus did not find any beneficial mutations there's only one rational conclusion: Wells was deliberately misrepresenting the truth.

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[Photo Credit: Jonathan Wells from Conservapedia]

Way to Heaven

 
This woman was greeting people at the subway stop outside of the Pharmacy Building on the university campus. You don't see this very much aroound here so I thought I take a picture.

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Parliament

 
I was cleaning up the photos on my cellphone and I found this. The buildings in the background are Canada's Parliament Buildings on "the hill." It's where all the MP's elected on Tuesday will be meeting in a few weeks. Does anyone recognize where I was when I took the picture?

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Tangled Bank #116

 
The latest issue of Tangled Bank has been published on Pro-Science [116th Tangled Bank].

Welcome to the 116th edition of the Tangled Bank. As usually, we have a lot of good stuff for you all. Unlike some former hosts, I am not a very creative writer, and I'll spare you all from any attempts of making some kind of theme for this Tangled Bank. So, without any further ado, let's get to the posts.

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Send an email message to host@tangledbank.net if you want to submit an article to Tangled Bank. Be sure to include the words "Tangled Bank" in the subject line. Remember that this carnival only accepts one submission per week from each blogger.

Balancer Chromosomes

Monday's Molecule #92 was a depiction of an inversion in a Drosophila chromosome (right).

The chromosomes shown here are the large polytene chromosomes of the salivary glands. They are made up of 1000-2000 aligned stands of DNA that form when successive rounds of DNA replication are not followed by separation of cell division. Flies that are heterozygous for a wild type chromosome and one with a large deletion inversion, will form the loop structure shown in the diagram.

In normal cells, you won't see this structure as the chromosomes align during mitosis and meiosis, but it still exists. What the structure tells us is that the presence of an inversion, or any other type of chromosomal rearrangement for that matter, doesn't have much effect on chromosomal alignment and segregation during cell division.

Today we want to focus on another point. Imagine that a recombination event (crossover) occurs when the chromosomes are aligned like this. If the crossover takes place in the inverted region then each of the recombined chromosomes will be missing some genes and the cells that are produced from such an event will die.

Imagine that the crossover occurs between point C and D. If we trace the new chromosome staring from A on the black chromosome (the AR chromosome) then you get A B G F E D on the black chromosome followed by C B A on the normal white chromosome. The other product of the crossover will begin with A B C from the normal white chromosome and end with D E F G B A from the black homologue.

There won't be any viable crossovers in the region covered by the mutation. We will see what this has to do with balancer chromosomes in a minute.

Imagine that you are working with an important mutation (x) that affects embryonic development in Drosophila. Flies that are homozygous for the mutation (x/x) are blocked at a particular stage of development and the visible phenotype of the mutations tells you a great deal about the genes that control development. These mutations are recessive lethals. The heterozygous flies with one mutant chrmosomes and one normal chromosome (x/+) are viable.

You want to maintain a stock of these flies so you can have mutant flies whenever you need to do an experiment. If you put a heterozygous male and female together in a fly bottle and leave them for a few weeks, you won't be surprised to find that there are no flies that are homozygous for the lethal mutation. However, repeated crossings of heterozygotes will result in 25% wild-type flies (+/+) and these flies will continue to mate with each other and with the heterozygous flies. You won't be able to tell which flies carry your valuable mutation.

One way around this is to mark your mutant chromosomes with a visible marker. Let's say that your mutation is on chromosome 2. (There are three autosomes and one pair of sex chromosomes in Drosophila.) You will need a dominant marker for reasons that will soon become apparent so let's choose detached (Dt), a mutation that effects the vein pattern on the wings. The chromosome carrying your valuable developmental mutation (x) will also carry the Dt allele.

Now all you have to do is look in your stock bottle for flies with the detached phenotype and you know that those flies should be heterozygous for x (Dt x/+ +). Flies that have normal wings can be recognized and killed. (Drosophila genetics is the ultimate blood sport.)

Problem solved, right?

No. It won't be long before a recombination event separates Dt and x, especially if they are far apart on chromosome 2. After a while you still won't know which flies carry your valuable mutation.

This is where balancers come in handy.

Let's look at the experiment done by Christiane Nüsslein-Volhard and Eric Wieschaus in the late 1970's. This is the experiment that won them the Nobel Prize.

In one of their experiments they were looking for mutations on chromosome 2 that affected embryo development.

They started with a line of flies that had eye color markers on chromosome 2; cinnabar (cn) and (bw). This is the red chromosome in the diagram. They treated males from this line with the potent mutagen ethyl methanesulfonate (EMS) and crossed them to a strain carrying a balancer chromosome (black) and a non-balancer homologous chromosome (blue).

The balancer chromosome is called CyO and it has several interesting features. First, it has a large inversion called In(2LR)O that covers most of the chromosome leaving only the ends intact. Second, it carries a dominant mutation called Curly (Cu) that produces flies with curly wings. This is a homozygous lethal mutation. Third, it carries another homozygous lethal mutation called dumpy-lethal (dp^1vI). Finally it carries cn. (Also purple (pr).)

The blue chromosome carries an allele called DTS-91. DTS stands for dominant temperature sensitive. Flies that carry even a single copy of this alleles will die at high temperature. DTS also stand for David T. Suzuki, the man who created these alleles but that's just a coincidence.

The first cross is done at high temperature. The flies produced from the first cross are the F1 generation. None of them will carry the blue chromosome because those flies will be killed at high temperature. All of them will carry one mutagenized chromosome 2 and the CyO balancer chromosome. These flies are crossed again with DTS-91/CyO flies at high temperature to get the second generation (F2) of flies that all contain one mutagenized chromosome 2 and CyO. The second cross helps eliminate other mutagenized chromsomes so that the workers will only be looking at mutations that affect chromosome 2.

Now the cn x bw/CyO flies are allowed to mate with each other until it's time to look at the effect of the mutations. The stock will never produce homozygous cn bw flies as long as the mutated chromosome carries a recessive lethal. Stocks that have flies with cinnibar eyes and not curly wings are discarded.

The stock will never produce flies that are homozygous for the balancer chromosome since it carries two recessive lethal mutations. All flies will have curly wings because they carry the balancer chromosome with Cu. There will never be a recombination event that transfers the developmental mutation to the balancer because the balancer contains a large deletion inversion.

This is why balancer chromosomes are so important n Drosophila genetics. They are essential for maintaining fly stocks carrying homozygous lethal mutations. Such mutations have been extremely important in sorting out fly development.

Christiane Nüsslein-Volhard and Eric Wieschaus created thousands of lines carrying recessive lethal mutations on chromosome 2, and thousands on the X chromosome and chromosome 3, each of which have their own balancers. Then they examined each line to look for embryos that were blocked during early development. (25% of the eggs will be homozygous for the mutant chromosome.)

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[Lower Figure credit: St Johnston (2002)]

St. Johnston, D. (2002) THE ART AND DESIGN OF
GENETIC SCREENS: DROSOPHILA MELANOGASTERNature Reviews: Genetics 3:178-188. [PDF]

Nobel Laureates: Christiane Nüsslein-Volhard and Eric Wieschaus

 

The Nobel Prize in Physiology or Medicine 1995.

"for their discoveries concerning the genetic control of early embryonic development"

Christiane Nüsslein-Volhard (1942 - ) and Eric F. Wieschaus (1947 - ) received the Nobel Prize in Physiology or Medicine for their contribution to understanding the genetics of development in the fruit fly, Drosophila melanogaster.

Their main contribution was to identify a number of genes that controlled the development of the embryo. The approach was to create mutations at random then screen large numbers of flies for recessive lethals affecting various stages of early embryogenesis. The initial large scale experiment was carried out at the EMBL Labs in Heidleberg, Germany. They established 27,000 lines containing mutated chromosomes and characterized 139 mutations affecting embryogenesis. Of these, 15 were described in the classic 1980 Nature paper. (See Silver Screen, a tribute to the paper on it's 25th anniversary.)

The original 15 genes were: cubitus interruptus, wingless, gooseberry, hedgehog, fused, patch, paired, even-skipped, odd-skipped, barrel, runt, engrailed, Kruppel, knirps, and hunchback. To anyone familiar with the field this reads like a who's who of Drosophila development. Dozens (hundreds?) of papers have been published on each of these genes.

The experimental approach is described in the Press Release below. I am only including the part that refers to Nüsslein-Volhard and Wieschaus. They shared the prize with Edward Lewis.

THEME:
Nobel Laureates

Brave decision by two young scientists

Christiane Nüsslein-Volhard and Eric Wieschaus both finished their basic scientific training at the end of the seventies. They were offered their first independent research positions at the European Molecular Biology Laboratory (EMBL) in Heidelberg. They knew each other before they arrived in Heidelberg because of their common interest: they both wanted to find out how the newly fertilized Drosophila egg developed into a segmented embryo. The reason they chose the fruit fly is that embryonic development is very fast. Within 9 days from fertilization the egg develops into an embryo, then a larvae and then into a complete fly.

Fig. 1 Regions of activity in the embryo for the genes belonging to the gap, pair-rule, and segment-polarity groups. The gap genes start to act in the very early embryo (A) to specify an initial segmentation (B). The pair-rule genes specify the 14 final segments (C) of the embryo under the influence of the gap genes. These segments later acquire a head-to-tail polarity due to the segment polarity genes.

They decided to join forces to identify the genes which control the early phase of this process. It was a brave decision by two young scientists at the beginning of their scientific careers. Nobody before had done anything similar and the chances of success were very uncertain. For one, the number of genes involved might be very great. But they got started. Their experimental strategy was unique and well planned. They treated flies with mutagenic substances so as to damage (mutate) approximately half of the Drosophila genes at random (saturation mutagenesis). They then studied genes which, if mutated would cause disturbances in the formation of a body axis or in the segmentation pattern. Using a microscope where two persons could simultaneously examine the same embryo they analyzed and classified a large number of malformations caused by mutations in genes controlling early embryonic development. For more than a year the two scientists sat opposite each other examining Drosophila embryos resulting from genetic crosses of mutant Drosophila strains. They were able to identify 15 different genes which, if mutated, would cause defects in segmentation. The genes could be classified with respect to the order in which they were important during development and how mutations affected segmentation. Gap genes (Fig 1) control the body plan along the head-tail axis. Loss of gap gene function results in a reduced number of body segments. Pair rule genes affect every second body segment: loss of a gene known as "even-skipped" results in an embryo consisting only of odd numbered segments. A third class of genes called segment polarity genes affect the head-to-tail polarity of individual segments.

The results of Nüsslein-Volhard and Wieschaus were first published in the English scientific journal Nature during the fall of 1980. They received a lot of attention among developmental biologists and for several reasons. The strategy used by the two young scientists was novel. It established that genes controlling development could be systematically identified. The number of genes involved was limited and they could be classified into specific functional groups. This encouraged a number of other scientists to look for developmental genes in other species. In a fairly short time it was possible to show that similar or identical genes existed also in higher organisms and in man. It has also been demonstrated that they perform similar functions during development.

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[Photo Credits: Nüsslein-Volhard - Encylopaedia Britanica, © Patrick Piel/Gamma Liaison, Wieschaus -News at Princeton]

Fair Vote Canada Election Results

 
Here's what the result would have been with a nation-wide proportional system from Fair Vote Canada.

Conservatives - 38% of the popular vote: 117 seats (not 143)
Liberals - 26% of the popular vote: 81 seats (not 76)
NDP - 18% of the popular vote: 57 seats (not 37)
Bloc - 10% of the popular vote: 28 seats (not 50)
Greens - 7% of the popular vote: 23 seats (not 0)

I don't favor such a system. I like the Mixed Member Proportional MMP) system based on provinces.

The British Columbia referendum on the Single Transferable Vote (STV) system for provincial elections is set for May 12, 2009. 58% of voters supported the new voting system in the last referendum (2005). This was just short of the required 60%. It is very likely that the new proportional system will be adopted this time around, making British Columbia the first of many provinces to enter the 21st century.

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Nigeria Has Competition

 
I just got this email message and I thought I'd share it with the rest of you. All my money is tied up in deals with Nigerians and investments in Viagra so I can't take advantage of this fabulous offer.

I expect to be flush with cash by next week because I just won the European lottery but I'll be spending most of it to enlarge one of my vital organs.

Hello Pal,

I hope my email fine you well. I am in need of your assistance. My name is Sgt. Jarvis Reeves. I am an American soldier serving in the 1st Armored Division in Iraq, we have just been posted out of Iraq and to return in a short while. My colleague and I need your help to transfer out the sum of Twenty Five Mllion U.S Dollars ($25 MUSD). If you are interested I will furnish you with more details

As awair your response.
Email:sgt.jr@hotmail.com

Yours,
Sgt. Jarvis Reeves

God Bless America!!

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Move to Canada

 

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[Hat Tip: The Unexamined Life]

Bacteria Phylogeny: Facing Up to the Problems

There are millions of species of bacteria. Sorting out their evolutionary history has been a major challenge for decades. Unlike the much bigger, multicellular, eukaryotes, there are few morphological markers to assist scientists in classifying bacteria. The fossil record is mostly silent.

Molecular evolution came to the rescue thirty years ago when cloning and sequencing became common. Soon there were elaborate and detailed phylogenetic trees based on comparing sequences of conserved genes from many species.

The gene of choice was the one for the small subunit ribosomal RNA (SSU rRNA). This gene was well conserved in bacteria and it was easy to get sequences simply by PCR. (The ends of the SSU rRNA gene are conserved and this means that you can develop universe primers for PCR.)

Over the years, the SSU rRNA gene has become what is called the "gold standard" in bacterial phylogeny and taxonomy. Many species have been assigned to taxa based entirely on the sequence of their SSU rRNA gene. Unfortunately, the "gold standard" has become somewhat tarnished lately.

Our fellow blogger, Jonathan Eisen of The Tree of Life, has recently published a paper that looks at the problems with bacterial phylogeny (Wu and Eisen, 2008). He posted a brief summary of the paper and commented on why he likes the journal Genome Biology [Happy Open Access Day: Back to Genome Biology for Me].

There is much to like about this paper. The authors face up to the problems with the current bacterial phylogeny, which is based almost entirely on a single gene (SSU rRNA). They point out that this is risky given what we know about molecular phylogenies. Furthermore, in the case of the SSU ribosomal RNA gene we know for a fact that this has led to problems and inconsistencies. In addition to the practical difficulties there are good theoretical reasons for being suspicious of phylogenies constructed from nucleotide sequences.

What to do? One possible solution is to abandon SSU rRNA as a "gold standard" and replace it with a highly conserved protein coding gene. Unfortunately, this doesn't get around the problem of relying on a single gene. The way around this is to use an artificial concatenated sequence made up of several different conserved genes laid out end-to-end in one large string of amino acids.

So why isn't this done? Because, as Wu and Eisen point out, it ain't that easy. The main difficulty in any phylogenetic study is getting a proper alignment. This is a problem that many workers simply ignore when they use automated alignment software like CLUSTALW. These workers assume that the alignments are valid.

They aren't, and this is another example of facing up to the problem. Many scientists agonize over what program to use when constructing their trees—should they use maximum likelihood, parsimony, etc. etc.? In most cases these decisions are a complete waste of time because their alignments aren't good enough to make a difference.

Here's how Wu and Eisen explain it ...

It has been shown that alignment quality can have greater impact on the final tree than does the tree-building method employed [20]. Therefore, preparing high quality sequence alignments is a most critical part of any molecular phylogenetic analysis. This preparation typically involves careful but tedious manual editing and trimming of the generated alignments, and thus remains the biggest challenge to automation. When scaling up this process, the trimming step is often simply ignored. Automated trimming based on the number of gaps in each column or each column's conservation score can be used to select conserved blocks, but still is not satisfactory when a high quality tree is required.

Keep in mind that what is being proposed is a large tree based on concatenated sequences from many genes. You don't want to do multiple sequence alignments for every gene by hand, and yet up until now, that was the only way to get accurate results.

Wu and Eisen have written a program called AMPHORA that hopefully solves this problem. They begin by manually creating "seed alignments" that are manually curated. Then they use AMPHORA to align all the other sequences to the seed alignments. In this way they hope to overcome the limitations of automated multisequence alignment without having to align everything by hand.

None of this would be possible, of course, unless there were large numbers of species where every one of the target genes have been cloned and sequenced. In the 20th century this would have been impossible but now there are hundreds of completely sequenced bacterial genomes. This means that each one of them has a sequenced copy of the genes required for this kind of analysis.

All that's left is to identify the completely sequenced genomes and pick the set of genes. There are 578 genomes in the database but many of these are close relatives that will not be useful in constructing a large tree of all bacterial sequences. The final set contains 310 genomes with representatives of all the major groups.

The authors selected 31 genes for their initial proof of principle paper (dnaG, frr, infC, nusA, pgk, pyrG, rplA, rplB, rplC, rplD, rplE, rplF, rplK, rplL, rplM, rplN, rplP, rplS, rplT, rpmA, rpoB, rpsB, rpsC, rpsE, rpsI, rpsJ, rpsK, rpsM, rpsS, smpB, tsf). Those of you who recognize these genes will see that 21 of them are small ribosomal proteins. This was not the best choice, in my opinion, but the authors of the paper note that they are continuing the study by incorporating better genes such as HSP70 (dnaL) and EF-Tu (tufA). You can't just choose any conserved gene because it has to be present in most species and there are surprisingly few genes that meet that criterion.

After all that, what's the bottom line? The grand phylogeny is shown at the top of this posting. It resolves many groups that are unresolvable using the SSU rRNA tree. In some cases this tree reveals species that have been incorrectly assigned to higher taxa. These species will have to be reclassified if this result holds up.

The most important finding is that the method works and it yields trees with excellent resolution of the major bacterial taxa.

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Wu, Martin, Eisen, Jonathan (2008). A simple, fast, and accurate method of phylogenomic inference Genome Biology, 9:R151 [Genome Biology] [doi:10.1186/gb-2008-9-10-r151]

Gene Genie #38

 
The 38th edition of Gene Genie has been posted at ScienceRoll [Gene Genie: Back in Action!].

Gene Genie is the blog carnival of clinical genetics and personalized medicine. Enjoy the numerous posts and articles focusing on these interesting fields of medicine. We dedicate this carnival edition to genetic testing, SNP watch and DNA.

The beautiful logo was created by Ricardo at My Biotech Life.

The purpose of this carnival is to highlight the genetics of one particular species, Homo sapiens.

Here are all the previous editions .....

1. Scienceroll
2. Sciencesque
3. Genetics and Health
4. Sandwalk
5. Neurophilosophy
6. Scienceroll
7. Gene Sherpa
8. Eye on DNA
9. DNA Direct Talk
10. Genomicron
11. Med Journal Watch
12. My Biotech Life
13. The Genetic Genealogist
14. MicrobiologyBytes
15. Cancer Genetics
16. Neurophilosophy
17. The Gene Sherpa
18. Eye on DNA
19. Scienceroll
20. Bitesize Bio
21. BabyLab
22. Sandwalk
23. Scienceroll
24. biomarker-driven mental health 2.0
25. The Gene Sherpa
26. Sciencebase
27. DNA Direct Talk
28. Greg Laden’s Blog
29. My Biotech Life
30. Gene Expression
31. Adaptive Complexity
32. Highlight Health
33. Neurophilosophy
34. ScienceRoll
35. Microbiology Bytes
36. Human Genetic Disordrs
37. The Genetic Genealogist
38. ScienceRoll

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Have Fun on Voting Day

 
Here's a video to keep you happy as you hold your nose and go to the polls (in Canada). There's a metaphor in it somewhere but I can't for the life of me figure it out. Maybe it has something to do with where my vote is going?

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[Hat Tip: psa at Canadian Cynic. Jennifer Smith at Runesmith's Canadian Content had the same idea I had about linking the video to voting day.]

PZ Myers in Toronto

 
Email me if you would like to meet PZ before his talk on Friday afternoon.

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Strategic Voting

 
Damn.

The Canadian election is tomorrow and I had almost made up my mind to vote for the Liberal candidate in my riding. He's a man I can respect and he will be a much better member of parliament than the Conservative candidate.

Up until last week I was considering a vote for the New Democratic Party because their policies are close to my personal position. Also, I wanted to send a message to Stéphane Dion, who I don't think is up to the job as leader of the Liberal party. I realized that my vote might result in the election of the Conservative candidate in my riding since the race between the Conservative challenger and Liberal incumbent is very close. That risk was worth it, in my opinion, because Stéphane Dion needed to lose in order to resign from the leadership.

The latest poll results indicate that the Conservatives might win a majority and I don't want that to happen. So I decided to vote Liberal, hoping that the events of the election campaign would be enough for Stéphane Dion. When he loses tomorrow he will resign.

At least that's what I thought until I read this morning's newspapers [The Canadian Press].

"I will never quit. I will stay for my country," the Liberal leader said Sunday during a last swing through southeastern Ontario before flying off on a frenetic coast-to-coast tour seeking the NDP and Green votes he desperately needs.

"But I'm working hard now. We're working all of us for a victory, for a progressive government. This is what is at stake."

When pressed on how he would respond if Liberal rivals push to oust him, a chippy Dion raised his voice.

"I'm the leader! I am the leader. And I'm working to win. I'm not a quitter."

...

Dion's strident tone may raise eyebrows in Liberal circles where private reaction to his campaign performance has typically ranged from tepid praise to hand wringing. Dion, a political scientist and former professor of public administration, has a reputation for tenacity and a mile-wide stubborn streak.

He is set to face a Liberal party leadership review next spring.

That's it for me. I'm voting NDP and I'm going to tell my Liberal candidate exactly why I'm doing it. If the only way to save the Liberal party is for Dion to quit ASAP and if the only way that will happen is if he's kicked out, then it looks like the Liberals are going to have to lose a lot of seats before they get the message.

I'll suffer the short term pain for the long term gain.

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Monday's Molecule #92

 
Today's molecule is a cartoon drawing of an image that depicts something very important. Your task is to explain what the image shows. Then you have to explain why this is important when it comes to describing the function of something called a "balancer."

It's a short step from there to this weeks Nobel Laureates. They used balancers in their work.

You need to describe what you see in the cartoon as accurately as possible and name the species. Then identify the Nobel Laureates, taking care to name only those ones who might have used balancers in their prize winnning work.

The first one to correctly identify the molecule 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 three ineligible candidates for this week's reward. You know who you are.

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: This weeks winner is Bill Chaney from Nebraska. He recognized that the "molecule" depicted a chromosomal inversion in a Drosophila chromosome. Such inversions are a characteristic of balancer chromosomes. Balancers are used in maintaining fly stocks, especially ones carrying homozygous lethal mutations.

The Nobel Laureates must be Christiane Nüsslein-Volhard and Eric Wieschaus

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Are Science and Religion Compatible?

 
I've been somewhat remiss in posting for a few days as I've been catching up on some reading and discussing science and religion with my friends.

The question that interests me is whether basic religious tenets are compatible with science, where "science" is defined as a way of knowing—a way that combines evidence and rational thinking to come up with "truths" about the universe we inhabit.

It seems obvious to me that there are some forms of deism that do not conflict with science. Is that it?¹ Are there any other versions of religion that maintain an appropriate distance from science?

I'd like to hear from people who are religious but not deists. Can they give me some example of their religious claims that do not in any way conflict with science? I'm thinking specifically of those religions that promote belief in a personal God.

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1. Buddhism may count if it's the form of Buddhism that doesn't believe in supernatural beings. I don't call that a religion.

Activist Scientists

 
We seem to have forgotten that scientists can be social activists. In my time it was common for scientist to take an active role in social causes. It was the time of "Science for the People" and similar organizations. Very little remains of that kind of activism, David Suzuki is just about the only one of those scientists who is still trying to change the world. Some of them have become administrators and advisers to Presidents.

Given the antagonism that greets modern scientists who step out of line (i.e., Richard Dawkins) I can understand why social activism is out of favor.

I was reminded that in the early part of the last century, there were scientists who took up social causes. I happened to stumble on the website of my colleague, Donald Forsdyke of Queen's University [Haldane's Rule]. Here's one of the photographs from that site.

JBS Haldane addressing a 'United Front' meeting in January 1937. Photograph from the Sun newspaper reproduced in Ronald Clark's 1968 biography of Haldane, published by Hodder & Stoughton.

It's hard to picture any of today's most prominent scientist in such a scene. Perhaps the "United Front" movement¹ is too liberal for the average scienist?

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1. It was a socialist movement with strong ties to Marxism as a philosophy and communism as an economic and political strategy

Why Do We Call them IDiots? (Part CCCLXVII)

 
Rebecca of Skepchick writes about a YouTube fight involving a creationist.

You know what’s hilarious? Seeing a jerk get schooled. You know what’s even funnier? When the jerk happens to be a creationist who has spent a lot of time and effort filling YouTube with the same old oft-debunked creationist garbage we see all the time, and who then illegally attempts to silence his rational critics.

I’ve been following the fight between creationist VenomFangX and pure awesomeness Thunderf00t for quite some time. For an overview, watch some of Thunderf00t’s excellent series, “Why Do People Laugh at Creationists?” VFX shows up a LOT. This upset him quite a bit.

Basically, VFX filed DMCA takedown notices on Thunderf00t’s videos, despite the fact that VFX knew those notices were false and malicious. This is illegal, and Thunderf00t obtained clear proof of the action. He could have sued the living pants off VFX and had him banned permanently from YouTube, but instead, he did this:

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Epigenetics, Again

 
The National Institutes of Health (NIH) have launched a $190 million research effort to learn about epigenetics. According to Nature News ...
It’s not that epigenetics is totally useless. I just don’t see why it’s worth 190 million dollars.

Kevin Struhl
Harvard Medical School

Epigenetics, described as "inheritance, but not as we know it"1, is now a blisteringly hot field. It is concerned with changes in gene expression that are typically inherited, but not caused by changes in gene sequence. In theory, epigenetic studies can help explain how the millions of cells in the human body can carry identical DNA but form completely different cell types, and perhaps why certain cells are susceptible to disease.

The NIH's epigenomics initiative is a plan for such studies on a grand scale including, for example, surveys in different human cell types of all the chemical tags, or epigenetic marks, that might control genes.

It seems strange to be spending so much research money on something that scientists can't even define properly [Epigenetics in New Scientist, Epigenetics Revisited, Epigenetics]. Perhaps some of this money will go toward coming up with a reasonable definition of what they're studying.

As far as I know we already have a good model for how totipotent cells can differentiate into many different cell types. We also understand how they can revert to pleuripotent cells. We even know that differentiated cells can be transformed back into stem cells by adding certain transcription factors.

Now we add in the fact that some DNA binding proteins can covalently modify DNA and this affects gene expression. What's the big deal?

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Humanism Is "Liberal"

 
I'm not a humanist and now I know why. Not only is it immoral and atheist but it's also (gasp!) LIBERAL! Now I know why the Christians are so frightened.

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[Hat Tip: Friendly Atheists]

P.S. I don't make fun of spelling errors because people in glass houses ....

P.P.S. As strange as it may seem to our neighbors to the south, in Canada we not only have a Liberal Party but people actually vote for it!

Nobel Laureate: Stanley Prusiner

 

The Nobel Prize in Physiology or Medicine 1997.

"for his discovery of Prions - a new biological principle of infection"

Stanley B. Prusiner (1942 - ) received the Nobel Prize in Physiology or Medicine for demonstrating that the prion protein was responsible for Creutzfeldt-Jakob disease (CJD) in humans and for scrapie in sheep. The significance of this work was that Prusiner rigorously eliminated any trace of RNA and DNA from the preparation of infectious disease particles. He showed for the first time that a protein cold be an infectious agent.

This was a major advance in our understanding of basic biological processes. It led to the discovery that a single protein could adopt two very different folds and one of them could induce folding changes in its neighbors in a catalytic manner. The discovery helps us understand protein folding and chaperones.

THEME:
Nobel LaureatesThe press release from the Nobel Prize website does a good job of describing Pusiner's contribution.

6 October 1997

The Nobel Assembly at the Karolinska Institute has today decided to award the Nobel Prize in Physiology or Medicine for 1997 to

Stanley B. Prusiner

for his discovery of "Prions - a new biological principle of infection".

Summary

The 1997 Nobel Prize in Physiology or Medicine is awarded to the American Stanley Prusiner for his pioneering discovery of an entirely new genre of disease-causing agents and the elucidation of the underlying priciples of their mode of action. Stanley Prusiner has added prions to the list of well known infectious agents including bacteria, viruses, fungi and parasites. Prions exist normally as innocuous cellular proteins, however, prions possess an innate capacity to convert their structures into highly stabile conformations that ultimately result in the formation of harmful particles, the causative agents of several deadly brain diseases of the dementia type in humans and animals. Prion diseases may be inherited, laterally transmitted, or occur spontaneously. Regions within diseased brains have a characteristic porous and spongy appearance, evidence of extensive nerve cell death, and affected individuals exhibit neurological symptoms including impaired muscle control, loss of mental acuity, memory loss and insomnia. Stanley Prusiner's discovery provides important insights that may furnish the basis to understand the biological mechanisms underlying other types of dementia-related diseases, for example Alzheimer's disease, and establishes a foundation for drug development and new types of medical treatment strategies.

The prize winning research was initiated 25 years ago

In 1972 Stanley Prusiner began his work after one of his patients died of dementia resulting from Creutzfeldt-Jakob disease (CJD). It had previously been shown that CJD, kuru, and scrapie, a similar disease affecting sheep, could be transmitted through extracts of diseased brains. There were many theories regarding the nature of the infectious agent, including one that postulated that the infectious agent lacked nucleic acid, a sensational hypothesis since at the time all known infectious agents contained the hereditary material DNA or RNA. Prusiner took up the challenge to precisely identify the infectious agent and ten years later in 1982 he and his colleagues successfully produced a preparation derived from diseased hamster brains that contained a single infectious agent. All experimental evidence indicated that the infectious agent was comprised of a single protein, and Prusiner named this protein a prion, an acronym derived from "proteinaceous infectious particle." It should be noted that the scientific community greeted this discovery with great skepticism, however, an unwavering Prusiner continued the arduous task to define the precise nature of this novel infectious agent.

The infectious prion particle forms within the body

Where was the gene encoding the prion, the piece of DNA that determined the sequence of the amino acids comprising the prion protein? Perhaps the gene was closely associated with the protein itself as in a small virus? The answers to these questions came in 1984 when Prusiner and colleagues isolated a gene probe and subsequently showed that the prion gene was found in all animals tested, including man. This startling finding raised even more questions. Could prions really be the causative agent of several dementia-type brain diseases when the gene was endogenous to all mammals? Prusiner must have made a mistake! The solution to this problem became evident with the sensational discovery that the prion protein, designated PrP, could fold into two distinct conformations, one that resulted in disease (scrapie PrP = PrPSc) and the other normal (PrP = PrPc). It was subsequently shown that the disease-causing prion protein had infectious properties and could initiate a chain reaction so that normal PrPc protein is converted into the more stabile PrPSc form. The PrPSc prion protein is extremely stabile and is resistant to proteolysis, organic solvents and high temperatures (even greater than 100o C). With time, non-symptomatic incubation periods vary from months to years, the disease-causing PrPSc can accumulate to levels that result in brain tissue damage. In analogy to a well known literary work, the normal PrPc can be compared to the friendly Dr. Jekyll and the disease causing PrPSc to the dangerous Mr. Hyde, the same entity but in two different manifestations.

Mutations in the prion gene cause hereditary brain diseases

The long incubation time for prion based disease hampered the initial efforts to purify the prion protein. In order to assess purification schemes Prusiner was forced to use scores of mice and in each experiment wait patiently for approximately 200 days for the appearance of disease symptoms. The purification efforts accelerated when it was demonstrated that scrapie could be transferred to hamsters, animals that exhibited markedly shortened incubation times. Together with other scientists, Prusiner cloned the prion gene and demonstrated that the normal prion protein was an ordinary component of white blood cells (lymphocytes) and was found in many other tissues as well. Normal prion proteins are particularly abundant on the surface of nerve cells in the brain. Prusiner found that the hereditary forms of prion diseases, CJD and GSS (see the last section), were due to mutations in the prion gene. Proof that these mutations caused disease was obtained when the mutant genes were introduced into the germline of mice. These transgenic mice came down with a scrapie-like disease. In 1992 prion researchers obtained conclusive evidence for the role of the prion protein in the pathogenesis of brain disease when they managed to abolish the gene encoding the prion protein in mice, creating so called prion knock-out mice. These prion knock-out mice were found to be completely resistant to infection when exposed to disease-causing prion protein preparations. Importantly, when the prion gene was reintroduced into these knock-out mice, they once again became susceptible to infection. Strangely enough, mice lacking the prion gene are apparently healthy, suggesting that the normal prion protein is not an essential protein in mice, its role in the nervous system remains a mystery.
Structural variant disease-causing prions accumulate in different regions of the brain

Specific mutations within the prion gene give rise to structurally variant disease-causing prion proteins. These structural prion variants accumulate in different regions of the brain. Dependent upon the region of the brain that becomes infected, different symptoms, typical for the particular type of disease are evident. When the cerebellum is infected the ability to coordinate body movements declines. Memory and mental acuity are affected if the cerebral cortex is infected. Thalamus specific prions disturb sleep leading to insomnia, and prions infecting the brain stem primarily affect body movement.

Other dementias may have a similar background

Prusiner's pioneering work has opened new avenues for understanding the pathogenesis of more common dementia-type illnesses. For example, there are indications that Alzheimer's disease is caused when certain, non-prion, proteins undergo a conformational change that leads to the formation of harmful deposits or plaques in the brain. Prusiner's work has also established a theoretical basis for the treatment of prion diseases. It may be possible to develop pharmacological agents that prevent the conversion of harmless normal prion proteins to the disease-causing prion conformation.

Intrinsic defense mechanisms do not exist against prions

Prions are much smaller than viruses. The immune response does not react to prions since they are present as natural proteins from birth. They are not poisonous, but rather become deleterious only by converting into a structure that enables disease causing prion proteins to interact with one another forming thread-like structures and aggregates that ultimately destroy nerve cells. The mechanistic basis underlying prion protein aggregation and their cummulative destructive mechanism is still not well understood. In contrast to other infectious agents, prion particles are proteins and lack nucleic acid. The ability to transmit a prion infection from one species to another varies considerably and is dependent upon what is known as a species barrier. This barrier reflects how structurally related the prions of different species are.

Prion diseases in animals and man

Without exception, all known prion diseases lead to the death of those affected. There are, however, great variations in pre-symptomatic incubation times and how aggressively the disease progresses.

Scrapie, a prion disease of sheep, was first documented in Iceland during the 18th century. Scrapie was transferred to Scotland in the 1940s. Similar prion diseases are known to affect other animals, e.g., mink, cats, deer and moose.

Bovine Spongiform Encephalopathy (BSE) - Mad cow disease is a prion disease that has recently received a great deal of publicity. In England BSE was transmitted to cows through feedstuff supplemented with offals from scrapie-infected sheep. The BSE epidemic first became evident in 1985. Due to the long incubation time the epidemic did not peak until 1992. In this year alone roughly 37,000 animals were affected.

Kuru among the Fore-people in New Guinea was studied by Carleton Gajdusek (recipient of the 1976 Nobel Prize in Physiology or Medicine). Kuru was shown to be transmitted in connection with certain cannibalistic rituals and was thought to be due to an unidentified "slow virus". The infectious agent has now been identified as a prion. Duration of illness from first symptoms to death: 3 to 12 months.

Gertsmann-Sträussler-Scheinker (GSS) disease is a hereditary dementia resulting from a mutation in the gene encoding the human prion protein. Approximately 50 families with GSS mutations have been identified. Duration of illness from evidence of first symptoms to death: 2 to 6 years.

Fatal Familial Insomnia (FFI) is due to another mutation in the gene encoding the human prion protein. Nine families have been found that carry the FFI mutation. Duration of illness from evidence of first symptoms to death: roughly one year.

Creutzfeldt-Jakob Disease (CJD) affects about one in a million people. In 85-90% of the cases it has been shown that CJD occurs spontaneously. Ten to fifteen per cent of the CJD cases are caused by mutations in the prion protein gene. In rare instances CJD is the consequence of infection. Previously infections were transmitted through growth hormone preparations prepared from the pituitary gland of infected individuals, or brain membrane transplants. About 100 families are known carriers of CJD mutations. Duration of illness from evidence of first symptoms to death: roughly one year.

A new variant of CJD that may have arisen through BSE-transmission. Since 1995 about 20 patients have been identified that exhibit CJD-like symptoms. Psychological symptoms with depression have dominated, but involuntary muscle contractions and difficulties to walk are also common.

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[Photo Credits top: David Powers University of California, San Francisco, bottom: Prionii si bolile prionice]

The 2008 Nobel Prize in Chemistry

 
I'm not a big fan of giving out Nobel Prizes for technological achievements although I do recognize that some of them are noteworthy. This one goes too far in the direction of technology, in my opinion. The technique is useful and has led to many advances in the field but I don't think it's Nobel Prize work.

There were many other worthwhile candidates who made significant advances in the study of basic science, leading to a direct contribution to our understanding of how nature works. None of the names commonly discussed on the science blogs got the prize.

The Chemistry prize was announced today: The Nobel Prize in Chemistry 2008. Here's the press release from the Nobel Prize website.

8 October 2008

The Royal Swedish Academy of Sciences has decided to award the Nobel Prize in Chemistry for 2008 jointly to

Osamu Shimomura, Marine Biological Laboratory (MBL), Woods Hole, MA, USA and Boston University Medical School, MA, USA,

Martin Chalfie, Columbia University, New York, NY, USA

and

Roger Y. Tsien, University of California, San Diego, La Jolla, CA, USA

"for the discovery and development of the green fluorescent protein, GFP".

Glowing proteins – a guiding star for biochemistry

The remarkable brightly glowing green fluorescent protein, GFP, was first observed in the beautiful jellyfish, Aequorea victoria in 1962. Since then, this protein has become one of the most important tools used in contemporary bioscience. With the aid of GFP, researchers have developed ways to watch processes that were previously invisible, such as the development of nerve cells in the brain or how cancer cells spread.

Tens of thousands of different proteins reside in a living organism, controlling important chemical processes in minute detail. If this protein machinery malfunctions, illness and disease often follow. That is why it has been imperative for bioscience to map the role of different proteins in the body.

This year's Nobel Prize in Chemistry rewards the initial discovery of GFP and a series of important developments which have led to its use as a tagging tool in bioscience. By using DNA technology, researchers can now connect GFP to other interesting, but otherwise invisible, proteins. This glowing marker allows them to watch the movements, positions and interactions of the tagged proteins.

Researchers can also follow the fate of various cells with the help of GFP: nerve cell damage during Alzheimer's disease or how insulin-producing beta cells are created in the pancreas of a growing embryo. In one spectacular experiment, researchers succeeded in tagging different nerve cells in the brain of a mouse with a kaleidoscope of colours.

The story behind the discovery of GFP is one with the three Nobel Prize Laureates in the leading roles:

Osamu Shimomura first isolated GFP from the jellyfish Aequorea victoria, which drifts with the currents off the west coast of North America. He discovered that this protein glowed bright green under ultraviolet light.

Martin Chalfie demonstrated the value of GFP as a luminous genetic tag for various biological phenomena. In one of his first experiments, he coloured six individual cells in the transparent roundworm Caenorhabditis elegans with the aid of GFP.

Roger Y. Tsien contributed to our general understanding of how GFP fluoresces. He also extended the colour palette beyond green allowing researchers to give various proteins and cells different colours. This enables scientists to follow several different biological processes at the same time.

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[Photo Credit: GFP Glowing Genes]

Steve Jones Says Human Evolution Is Over

There's so much wrong with this article by Steve Jones that I don't know where to begin. So I'll leave it up to Sandwalk readers to comment. Steve Jones is a Professor of genetics at University College, London (UK) and the author of Darwin's Ghost.

From Times Online via RichardDawkins.net.

Leading geneticist Steve Jones says human evolution is over
By Julia Belluz

Human evolution is grinding to a halt because of a shortage of older fathers in the West, according to a leading genetics expert.

Fathers over the age of 35 are more likely to pass on mutations, according to Professor Steve Jones, of University College London.

Speaking today at a UCL lecture entitled "Human evolution is over" Professor Jones will argue that there were three components to evolution – natural selection, mutation and random change. "Quite unexpectedly, we have dropped the human mutation rate because of a change in reproductive patterns," Professor Jones told The Times.

"Human social change often changes our genetic future," he said, citing marriage patterns and contraception as examples. Although chemicals and radioactive pollution could alter genetics, one of the most important mutation triggers is advanced age in men.

This is because cell divisions in males increase with age. "Every time there is a cell division, there is a chance of a mistake, a mutation, an error," he said. "For a 29-year old father [the mean age of reproduction in the West] there are around 300 divisions between the sperm that made him and the one he passes on – each one with an opportunity to make mistakes.

"For a 50-year-old father, the figure is well over a thousand. A drop in the number of older fathers will thus have a major effect on the rate of mutation."

Professor Jones added: "In the old days, you would find one powerful man having hundreds of children." He cites the fecund Moulay Ismail of Morocco, who died in the 18th century, and is reputed to have fathered 888 children. To achieve this feat, Ismail is thought to have copulated with an average of about 1.2 women a day over 60 years.

Another factor is the weakening of natural selection. "In ancient times half our children would have died by the age of 20. Now, in the Western world, 98 per cent of them are surviving to 21."

Decreasing randomness is another contributing factor. "Humans are 10,000 times more common than we should be, according to the rules of the animal kingdom, and we have agriculture to thank for that. Without farming, the world population would probably have reached half a million by now – about the size of the population of Glasgow.

"Small populations which are isolated can evolve at random as genes are accidentally lost. World-wide, all populations are becoming connected and the opportunity for random change is dwindling. History is made in bed, but nowadays the beds are getting closer together. We are mixing into a glo-bal mass, and the future is brown."

Be sure to keep in mind the definition of evolution [What Is Evolution?].

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My Friend Publishes a Book

 
Many years ago I had a friend who lived just up the street. We didn't get to see each other very much because we went to different high schools. But we did go on one date—to a Simon and Garfunkel concert. It didn't make much of an impression on her because she doesn't even remember it!

Later on she became a well known radio and TV personality including a stint as the co-anchorwoman on the CBC National and a interviewer on "As It Happens" on CBC Radio and NPR.

Now she's written a book and I'm sure it's going to be an excellent read.

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Framing Science

 
Matt Nisbet recently posted the following message under the title Framing Science Ranked Among Top 15 Science Blogs.

For the fourth straight month, Framing Science ranks among the top 15 science-related blogs, as tracked by Wikio. The position of a blog in the Wikio ranking depends on the number and weight of the incoming links from other blogs. (Blogrolls are not taken into account and Wikio only counts links from the last 120 days.)

I submitted a comment in which I noted that several famous science blogs such as Bad Astronomy, The Panda's Thumb, and RichardDawkins.net are not included in the Wikio rankings.

Since this has been discussed many times on the blogs, it's safe to assume that Matt knows about it. I think he understands that his ranking among the top 15 blogs is not quite what it seems. So I asked in the comment whether he was deliberately trying to deceive his readers or was this an example of framing?

Unfortunately, my comment must have gone astray in the ether since it didn't survive moderation. Isn't that strange?

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