Gene and Transcription Orientation

 
The DNA double helix consists of two strands of DNA wound around each other to form the classic helical structure. One of the most important insights into solving the structure was when Watson and Crick realized that the two strands had to run in opposite direction. The ends of each strand are identified by the carbon atom on the deoxyribose sugar. One end is called the 5′ (five prime) end because the 5′ carbon atom is exposed. The other end is called the 3′ (three prime) end because the 3′ carbon atom is exposed.

RNA (and DNA) can only be synthesized from the 5′ to the 3′ direction. What this means is that at the beginning of the gene when the transcription bubble forms it's the template strand that's copied into RNA and the beginning of the template strand is the 3′ end. (It's the opposite orientation of the newly synthesized RNA.) [see Transcription]

The complementary strand of DNA is called the coding strand because it represents the sequence of the gene product. In other words, it's the same sequence as the RNA. By convention the orientation of the gene is determined by the coding strand and not the template strand. Thus, the beginning of a gene is called the 5′ end and the end of a gene is the 3′ end;.

The electron micrograph below shows E. coli ribosomal RNA genes being transcribed. The thin line (upper right) is the Double-stranded DNA strand. Transcription of the genes begins at the initiation site (lower left). This is the 5′ end of the genes.

RNA polymerase first bound to the initiation site and began transcribing in the 5′ to 3′ direction as shown. As the transcription complex moves along the gene the RNA product gets longer. In this case it is bound to protein so it looks compact. About halfway along the genes the RNA is processed by cutting and that's why it seems to get shorter near the middle of the gene.

The large ribosomal RNA is in the second half of the transcribed region. You can see that the RNA in the second half is larger than the small ribosomal RNA in the first half.

Note that there are many transcription complexes transcribing this region at the same time. In fact, they are about as closely packed as they can possibly be. These genes are being transcribed at the maximum possible rate. They have a very strong promoter.

Facts and Myths Concerning the Historical Estimates of the Number of Genes in the Human Genome

In April 2005 Gil Ast published an article in Scientific American (Ast, 2005). The title of the article was “The Alternative Genome” and its main point was how alternative splicing in humans could increase the number of different proteins that we produce. He explains why he thinks the proteome is so much larger than the number of genes. (Ast claims that there are 90,000 proteins and only 25,000 genes.)

Ast begins his argument with the quotation below.

Spring of 2000 found molecular biologists placing dollar bets. Trying to predict the number of genes that would be found in the human genome when the sequence of its DNA nucleotides was completed. Estimates at the time ranges as high as 153,000. ... given our complexity we ought to have a bigger genetic assortment than the 1000-cell roundworm, Caenorhabditis elegans, which has a 19,500-gene complement, or corn, with its 40,000 genes.

When a first draft of the human sequence was published the following summer, some observers were therefore shocked by the sequencing team’s calculation of 30,000 to 35,000 protein-coding genes. The low number seemed almost embarrassing.

Ast's remarks illustrate two points that I want to address. The first point is the surprise factor. Ast, and some other scientists, were surprised (and embarrassed) by the low gene count. They imply that most genome experts were also shocked when the genome sequence was published. That’s not quite correct, as I will show below.

The second point will have to be put off for another time but it’s important enough to mention here. Ast thinks that humans need to make many times more proteins than worms and corn because we are so much more complex. There are two problems with such a point of view—are we, in fact, 2-3 times more complex than corn? And, does it take thousands of new proteins to generate the structures that make us unique?

I think some people exaggerate our complexity and the place of humans relative to other species. This incorrect perspective can cause some scientists to put their faith in weakly supported hypotheses that claim to explain why humans really are complex and important in spite of the fact that we don’t have a lot of genes.

But let's put that discussion aside for a few days in order to discuss the historic estimates of the number of genes in the human genome. The statement by Gil Ast is typical of those who are embarrassed. They exaggerate the estimates of the total number of genes in order to make it look like everyone—not just them—thought there would be far more genes than the 25,000 that have been found. Just this month (March 2007) this myth was repeated by Taft et al. (2007).

Predictions of the estimated number of protein-coding genes in the human genome prior to genome sequencing ranged from as low as 50,000 to as high as 140,000, whereas the latest estimates from genome analysis indicate that humans have approximately 20,000 protein-coding genes.

The graphic above was taken from the Genesweep lottery. This is the betting that Asp refers to. It shows the range of gene number estimates by scientists who were involved in genome sequencing projects. Note that there are many estimates in the 40-50,000 range and a fair number below 40,000. The point is obvious—lots of experts anticipated fewer than 50,000 genes in the human genome (see The nature of the number. Nature Genetics 25:127 (2000)).

The earliest estimates of gene number are based on genetic load arguments (see King & Jukes, 1969). Since approximate mutation rates were known by 1960, it was possible to estimate the maximum number of genes that could be mutated without presenting an impossible genetic load. In other words, how many genes could we have before the number of lethal mutations per generation became intolerable? This number was less than 40,000 genes; an estimate that has never been refuted or discredited. Many experts were well aware of this upper bound up until the time the genome sequence was published.

By the 1970's there were good estimates of the total number of unique Drosophila melanogaster genes that could be mutated to lethality. The range was about 5,000-10,000 genes and this correlated well with the genetic map and the organization of polytene chromosomes. It was known that the Drosophila genome was much larger than the total size of the estimated number of genes but studies from a number of labs confirmed that a great deal of genomic DNA was repetitive junk DNA.

As we learned more and more about how genes controlled development, it became clear that huge differences in morphology and "complexity" could be due to very small changes in the either the number of regulatory genes or when they were expressed. Most of the people who assimilated the advances in developmental biology began to appreciate that mammals do not need to have many more genes than fruit flies.

By 1980, the amount of unique sequence DNA in mammalian genomes was known to be capable of encoding fewer than 20,000 genes if the average size of a gene was 10,000 bp (including introns). We now know that much of the intron sequences is not unique sequence DNA but that wasn't known back then. This estimate of gene number was consistent with detailed analysis of the amount of DNA that could be protected by mRNA or by Rot analysis (kinetics of hybridization of RNA to DNA). Mouse embryos (gastrula) appeared to express about 20,000 average-sized mRNAs. Some of these were present at very low abundance leading to the idea that this value may represent most of the mouse genes in the genome (summarized in Lewin, 1980). Certainly it was known that mammals expressed about 10,000 housekeeping genes in most cells and tissues. The general consensus was that the total number of regulatory genes was unlikely to be more than twice this number (probably less) for a total of 30,000 genes at most.

It was about this time that Walter Gilbert made his famous back-of-the-envelope calculation of 100,000 genes in the human genome. This was the estimate that became widely quoted when the human genome project was first proposed. It's interesting to note that Gilbert's estimate was not based on any experimental evidence; indeed, it conflicted with most of the available evidence suggesting far fewer genes. The larger number seemed less threatening to scientists who were worried that we might not have more genes than a fruit fly.

By the late-1990's we had estimates of the total number of human genes from the sequences of chromosomes 21 and 22 and from the sequence of a large contiguous region of the MHC locus. The results suggested fewer than 45,000 genes total—even less if these sequenced regions turned out to be gene rich as was widely suspected. Thus, the number of genes was coming out to be well below 50,000 and this was in line with the data from RNA hybridization studies and genetic load. It also fit with the concept that the number of genes in mammals was probably not more than twice the number in insects.

In contrast to these results, the estimates from expressed sequence tags (ESTs) were often much higher. Expressed sequence tags are short copies of RNA isolated directly from cells. The idea was that these represented bits of mRNA so each one revealed the presence of a protein-coding gene. As more and more ESTs were deposited in the sequence libraries, it became possible to estimate when the library would be complete and the totals were often more than 100,000 distinct mRNAs. For example, just before the human genome sequence was published, (Liang et al., 2000) estimated that there were 120,000 genes based on the analysis of 2 million EST's.

Not everyone believed in the validity of the EST data. There were some who thought that most ESTs were artifacts. They turned out to be correct although this is not widely appreciated. By using the sequences of chromosomes 21 and 22 as controls Ewing and Green (2000) were able to estimate 35,000 genes based on the EST libraries.

Thus, by the time the draft sequence was published in 2001 there were many scientists who anticipated that the number of genes would be less than 40,000 and that's why there are so many bets in that range in the Genesweep lottery. When the number of genes was announced to be about 30,000 there were many of us who were not the least bit surprised. The only ones who were surprised were those who ignored most of the data and clung to the idea humans had to have far more genes than the so-called "lower" species.

It is simply not true that all the experts were surprised at the low number of genes. Some experts were, but many were not. The interesting thing is that those who wanted there to be more genes have not given up the fight. They continue to publish rationalizations and just-so stories in an attempt to justify why they were wrong.

UPDATE:The latest estimates indicate that the human genome contains about 20,500 protein-encoding genes [Humans Have Only 20,500 Protein-Encoding Genes]. There are probably about 1500 genes for the known stable RNAs for a total of 22,000.

Ast,G. (2005) The alternative genome. Sci. Am. 292; 40-47.

Ewing,B. and Green,P. (2000) Analysis of expressed sequence tags indicates 35,000 human genes. Nat. Genet. 25; 232-234.

King,J.L. and Jukes,T.H. (1969) Non-Darwinian evolution. Science 164; 788-798.

Lewin, B. (1980) Gene Expression-2 2nd ed. Chapter 24; Complexity of mRNA Populations.

Liang,F., Holt,I., Pertea,G., Karamycheva,S., Salzberg,S.L., and Quackenbush,J. (2000) Gene index analysis of the human genome estimates approximately 120,000 genes. Nat. Genet. 25; 239-240.

What Is This?

 
Why it's Stenocereus eruca, of course.

Don't know what that is?

Find out if it's a plant, an animal, or something else entirely by going [here].

It (mostly) doesn't have sex but shows a fairly high level of genetic diversity.

Sex, genes & evolution

 
With a title like that how could you not want to read John Logsdon's new blog? Yesterday was his first post but I'm looking forward to lots more in the near future [Sex, Genes & Evolution].

John is a molecular evolutionary biologist in the Biology Department at the University of Iowa. He has published a number of papers with W. Ford Doolittle from the time he was at Dalhousie University in Nova Scotia. These include several papers with Arlin Stoltzfus on the evolution of introns. The Stoltzfus/Logsdon papers from this era were among the best papers to refute the intron-early hypothesis formerly championed by their mentor, Ford Doolittle. One of the things this demonstrates is that it's possible to disagree with your boss and survive!

Their chief target at the time was the Gilbert lab. John Logsdon was one of the participants in the famous online BioMedNet debate on The Origin and Evolution of Introns in November 1996—back in the time before blogs. This was mostly a debate between members of the Ford Doolittle lab and the Gilbert lab. Unfortunately, the transcript is no longer available. It was required reading in most molecular biology courses in the late 1990's. (I wish we had more debates like that.)

The Logsdon lab is interested in sex in protists, specifically the evolution of genes involved in recombination and meiosis (e.g., RAD51). John participates in a larger project that is trying to define the eukaryotic tree of life. As most of you know, the relationship of protists is controversial and the collaborative project intends to try and resolve the controversies. It not going to be easy to figure out the early history of eukaryotic evolution. This is a problem that has perplexed evolutionary biologists for several decades.

The Iowa biologists' goal is to sequence nine genes (actin, α- and β- tubulin, cob, EF-1 a , Hsp70, Hsp90, RPB1, SSU rRNA) from at least 200 different protists [ Assembling the Tree of Eukaryotic Microbial Diversity and Eu-Tree].

I'm excited about this project because they're looking at the best gene (HSP70). I hope he won't be disappointed to learn that my undergraduates have already solved the problem [The Evolution of the HSP70 Gene Family]. But all is not lost, those other genes might make a minor contribution to understanding evolution.

Welcome to science blogging, John.

Now, why not jump right in and describe your favorite hypothesis for why we have sex? I'm guessing you're a fan of repair, right?

Monday's Molecule #18

 
Name this molecule. You must be specific but we don't need the full correct scientific name. (If you know it then please post it.)

As usual, there's a connection between Monday's molecule and this Wednesday's Nobel Laureate. This one's very easy once you know the molecule. There'll be a few extra bonus points for guessing Wednesday's Nobel Laureate(s).

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

How Nerdy Am I?

 



[Hat Tip: Shalini.]

What Color Green Am I?

 

You Are Emerald Green

Deep and mysterious, it often seems like no one truly gets you. Inside, you are very emotional and moody - though you don't let it show. People usually have a strong reaction to you... profound love or deep hate. But you can even get those who hate you to come around. There's something naturally harmonious about you.

What Color Green Are You?

[Hat Tip: Monado]

A New Transitional Fossil

 
This is a new transitional fossil manmmal called Yanoconodon. It's from the Meozoic era (about 200 million years ago). The fossil tells us a great deal about mammalian evolution, especially the evolution of the jaw and ears. If you are interested in evolution you must read PZ Myers' excellent description of this fossil [Yanoconodon, a transitional fossil].

The creationist and intelligent design websites will soon be out with their own explanation of how this fossil fits with their version of the history of life. I'll link to them as soon as they post. If you spot these interpretations before I do, please let me know. I can't wait to see how they handle this news scientific evidence.

Meanwhile, congratulations PZ for a wonderful article.

Intelligent Design for Dummies

 
Do you understand Intelligent Design? Fear not, UK comedian Robin Ince explains it in a clip from the show "Comedy Cuts" aired March 15th on ITV in the UK. (Why can't there be more documentaries like this on TV in the USA?)



[Hat Tip: PZ Myers.]

Stéphane Dion Does Milton

 
Jennifer Smith has all the details over at Runesmith's Canadian Content [Dion Does Milton].

Sounds like it was a lot of fun. I hope he comes to my riding. It was the one formerly represented by Carolyn Parrish. But she was kicked out of the Liberal party so that's not quite the same as supporting a new Liberal like Garth Turner.

Happy St. Patricks Day!!!

 

Today's the day when the Irish—and people who want to be Irish—celebrate by doing typically Irish things; like drinking green beer, dancing Irish jigs, and going to mass. (?)

My ancestors on my mother's side are (mostly) Irish. My grandfather was a Doherty (O'Doherty). Thats the name at the top of the map in country Donegal. That side of the family came to Canada in 1802 and the Irish blood has been diluted—most notably by American refugees from the Revolutionary War (United Empire Loyalists) (gasp!).

The O'Doherty's are descended from Niall Noigíallach who kidnapped St. Patrick.

My grandmother was a Foster from Fermanagh. That's by the two lakes (Lower Lough Erne and Upper Lough Erne) in the upper central part of the country near the seat of the Maguires. Her family came to Canada in 1865 but both of her parents were Irish so at least 1/4 of my genes are undiluted Irish. I'll drink to that.

We don't talk about the nasty little fact that the Foster's were probably English invaders from the 1600's. As they say, somebody had to civilize the Irish and it might as well have been the English!

One of the reasons why the topic was avoided by my grandparents was because the O'Doherty clan was almost wiped out by the English during the O'Doherty rebellion in 1608 led by Sir Cahir O’Doherty. Some of the survivors had to flee to Skye to avoid being hung. I descend from those refugees.

Roundup® Is Safe

There have been dozens of studies on the possible harmful effects of Roundup®. There are many well-funded organizations and tons of lawyers who would like nothing better than to sue Monsanto into bankruptcy. Given the millions of farmers and suburban gardeners who slop Roundup® on themselves on a regular basis, you'd think it would be easy to come up with some who have died of cancer or, at least, suffered serious health problems.

Hasn't happened. Most of the scientific studies find no harmful effects of Roundup® on humans. Here's a bit from a study done for THE COMMONWEALTH OF MASSACHUSETTS in 2003.

TOXICITY REVIEW
Acute (Mammalian)
Glyphosate has reported oral LD5Os of 4,320 and 5,600 mg/kg in male and female rats (15,4). The oral LD5Os of the two major glyphosate products Rodeo and Roundup are 5,000 and 5,400 mg/kg in the rat (15). A dermal LD5O of 7,940 mg/kg has been determined in rabbits (15,4). There are reports of mild dermal irritation in rabbits (6), moderate eye irritation in rabbits (7), and possible phototoxicity in humans (9). The product involved in the phototoxicity study was Tumbleweed marketed by Murphys Limited UK (9). Maibach (1986) investigated the irritant and the photo irritant responses in individuals exposed to Roundup (41% glyphosate, water, and surfactant); Pinesol liquid, Johnson Baby Shampoo, and Ivory Liquid dishwashing detergent. The conclusion drawn was that glyphosate has less irritant potential than the Pinesol or the Ivory dishwashing liquid (120).
Metabolism
Elimination of glyphosate is rapid and very little of the material is metabolized (6,106).
Subchronic/Chronic Studies (Mammalian)
In subchronic tests, glyphosate was administered in the diet to dogs and rats at 200, 600, and 2,000 ppm for 90 days. A variety of toxicological endpoints were evaluated with no significant abnormalities reported (15,10). In other subchronic tests, rats received 0, 1,000, 5,000, or 20,000 ppm (57, 286, 1143 mg/kg) in the diet for 3 months. The no observable adverse effect level (NOAEL) was 20,000 ppm (1,143 mg/kg) (115). In the one year oral dog study, dogs received 20, 100, and 500 mg/kg/day. The no observable effect level (NOEL) was 500 mg/kg (116).

etc.

You may not like Monsanto and genetically-modified food for ethical reasons or because the company exploits third-world farmers. These are valid, if controversial, reasons for opposing the spread of genetically-modified crops. Personally I don't have a problem with genetically modified foods, but I do have a problem with the power of large international for-profit companies.

Express your opposition, if it's rational and scientifically based, but don't fall into the trap of opposing GM foods because you think Roundup® is dangerous. This kind of opposition (see below) is just plain silly. It is a superstitious, anti-science, way of thinking.

If You Think Monsanto's Roundup is a Safer Pesticide,
Please read the articles and papers on this page! Roundup is a pesticide as defined by the EPA.

If you're still not convinced that Roundup is a highly toxic and persistent pesticide, read on, while at the same time remembering the other contributions that Monsanto has made to society such as:

Saccharin, Astroturf, agent orange, dioxin, sulphuric acid, polychlorinated biphenyls (PCBs), plastics and synthetic fabrics, research on uranium for the Manhattan Project that led to the construction of nuclear bombs, styrene monomer, an endless line of pesticides and herbicides (Roundup), rBGH (recombinant bovine growth hormone that makes cows ill), genetically engineered crops (corn, potatoes, tomatoes, soy beans, cotton), and it's most significant product to date; Lies, Factual Distortions and Omissions.

[from Everything You Never Wanted to Know About Monsanto's Modus Operandi (M.O.)]

Glyphosate-resistant Weeds

Roundup® (glyphosate) has been used to control weeds since 1974 [How Roundup® Works]. In all those years, the number of reported cases of resistant plants has been far below predictions. Only in the past ten years have Roundup®-resistant plants been identified and there are only 11 species of resistant weeds known at last count (Perez-Jones et al. (2007).

We now know from studies of the mechanism of resistance of the C4 EPSP synthase that resistance to glyphosate requires very special circumstances; namely, an enzyme active site that can exclude glyphosate while still allowing phosphoenolpyruvate to bind efficiently [The Molecular Basis of Roundup® Resistance]. Thus, with hindsight, it is perhaps not surprising that so few resistant plants have turned up.

One of the first resistance mechanisms to be discovered was one that evolved in a population of goosegrass from Malaysia (Baerson et al. 2002). The glyphosate-resistant biotype (strain) was from a region that had been continuously sprayed for 10 years.

Baerson et al. (2007), working out of the Monsanto Labs in St. Louis MO (USA), discovered that the resistant strain of goosegrass was resistant to about five times the normal level of glyphosate. All of this resistance was apparently due to a single amino acid change in the active site of EPSP synthase. The substitution of a proline for a serine residue at position 106 decreased glyphosate binding without affecting phophoenolpyruvate binding.

Taken together, these studies suggest that an altered EPSPS provides a significant component of the glyphosate resistance mechanism in goosegrass, and represents the first example for target-based resistance to glyphosate occurring in any plant species.

The authors cannot explain why this P106S substitution confers resistance in the goosegrass enzyme, since similar substitutions in other plant enzymes affect substrate binding and render the enzyme ineffective. They conclude with,

It is possible that goosegrass may be predisposed to this type of mechanism due to species-specific genetic or physiological characteristics that remain obscure at present.

This has important implications for our understanding of evolution. Taken at face value, it suggests that in some species an evolutionary path is simply not available—there may not be a route to the so-called "top of the fitness peak." On the other hand, in other species a path can open up with a single mutation because that species, by chance, has the right kind of background. Evolution by accident.

Glyphosate-resistance has independently evolved in two strains of Italian ryegrass (Lolium multiflorum) from Oregon and Chile. The mechanism of resistance was studied by Perez-Jones et al. (2007). In this case there are two different mechanisms of resistance.

The strain from Chile had the same EPSP synthase mutation as that found in goosegrass (proline for serine at position 106). The Orgeon strain was defective in absorbing glyphosate in the roots suggesting a defect of some sort in absorption and/or transport. This is a new kind of resistance and it's not well understood at this time.

There have been rumors of Roundup® resistant coca plants in Bolivia—the ones whose leaves are used to produce cocaine. The rumors were so persistent that the magic crop was tested to see if it had been genetically engineered in a secret lab sponsored by the drug lords [The Mystery of the Coca Plant That Wouldn't Die]. The article reports that tests for C4 EPSP synthase were negative suggesting that the plants have acquired a natural resistance.

The implication is that the farmers' decentralized system of disseminating coca cuttings has been amazingly effective - more so than genetic engineering could hope to be. When one plant somewhere in the country demonstrated tolerance to glyphosate, cuttings were made and passed on to dealers and farmers, who could sell them quickly to farmers hoping to withstand the spraying. The best of the next generation was once again used for cuttings and distributed.

This technique - applied over four years - is now the most likely explanation for the arrival of Boliviana negra. By spraying so much territory, the US significantly increased the odds of generating beneficial mutations. There are numerous species of coca, further increasing the diversity of possible mutations. And in the Amazonian region, nature is particularly adaptive and resilient.

"I thought [genetic engineering] was unlikely," says Gressel, the plant scientist at the Weizmann Institute. "But farmers aren't dumb. They obviously spotted a lucky mutation and propagated the hell out of it."

The effects of this are far-reaching for American policymakers: A new herbicide would work only for a limited time against such a simple but effective ad hoc network. The coca-growing community is clearly primed to take advantage of any mutations.

From what we know of glyphosate resistance it seem unlikely that these Bolivian plants are actually resistant to Roundup®. It's probably just over-active imagination.

Baerson, S.R., Rodriguez, D.J., Tran, M., Feng, Y., Biest, N.A., Dill, G.M. (2002) Glyphosate-resistant goosegrass. Identification of a mutation in the target enzyme 5-enolpyruvylshikimate-3-phosphate synthase. Plant Physiol. 129:1265-1275. [PubMed]

Perez-Jones, A., Park K.W., Polge, N., Colquhoun, J., and Mallory-Smith, C.A. (2007) Investigating the mechanisms of glyphosate resistance in Lolium multiflorum. Planta. 2007 Feb 24 (electronic publication, ahead of print).

Wanna Speciate? Come to Canada

A recent Science paper by Wei and Schluter (2007) asks whether speciation rates really are faster in the tropics as widely believed. They looked at 309 sister species of mammals and birds in North and South America. Sister species are closely related species that have apparently diverged within the past few million years. The time since divergence was estimated by comparing the sequences of the mitochondrial cytochrome b gene. This gives an estimate of the rate of speciation by cladogenesis for each pair of sister species.

The range of each species was estimated from literature data and the time of speciation results were plotted in relation to the midpoint latitude of the range. The result was quite striking.

Near the equator, the ages of sister-species pairs spanned the past 10 million years, with a mean age of 3.4 million years ago. As the distance from the equator increased, the upper limit and mean ages of sister species declined significantly. At the highest latitudes, all of the sister species diverged less than 1.0 Ma.

It's widely known that there are far more species in the tropics than in temperate or arctic climates. How do we explain this apparent discrepancy?

Weir and Schluter (2007) estimated extinction rates at various latitudes and discovered that the rate of species extinction also increased with distance from the equator but the rate of increase was greater than the rate of increase in speciation. Thus, although there were more speciation events in temperate zones, there were also more extinctions, and the extinctions cancelled out the effect of frequent cladogenesis.

The net effect is more species in the tropics even though speciation rates are higher in temperate zones.

John Wilkins is an expert on species. He points out that there's no universal definition of species. I wonder if this result isn't biased by different ways of recognizing species. Perhaps populations and sub-species are more easily named in temperate zones because there's more room for them to spread out into non-overlapping ranges. Does anyone know whether "species" in temperate zones are more likely to be similar in appearance than in the tropics?

In any case, the result is intriguing. It suggests that things move pretty slowly in hot climates. If you want some fast speciation action you need to move north to a cooler place.

Weir, J.T. and Schluter, S. (2007) The Latitudinal Gradient in Recent Speciation and Extinction Rates of Birds and Mammals. Science 315: 1574-1576.

[Hat Tip: RichardDawkins.net; Cold is hot in evolution -- Researchers debunk belief species evolve faster in tropics]

St. Patrick Banished Snakes from Ireland

 
Friday's Urban Legend: FALSE

Connie Barlow describes A St. Patrick's Day Parable.

Ireland is a land of no snakes. It has no slithering serpents. There are no rat snakes in Ireland; there are no rattlesnakes; there are no garter snakes. There are no snakes at all.

The absence of snakes in Ireland seems to cry out for an explanation — but only if one regards or ventures to the island from outside: from England, say, or from continental Europe. To the indigenous Celts, there would, of course, have been nothing to explain. The Gaelic peoples no more needed to explain an absence of snakes on their island home than they needed to explain an absence of kangaroos. To those who came to Ireland from abroad, however, a dearth of serpents was a striking anomaly in need of an answer.

We humans must have answers. And so arose the legend of St. Patrick and the snakes. The reason Ireland has no snakes, the story goes, is that Patrick charmed all snakes on the island to come down to the seashore, slither into the water, and drown. So Ireland did once have snakes, but it has them no more. Patrick charmed them all into the sea.

She goes on to explain why there are no snakes in Ireland but I prefer to swtich to the website of the Smithsonian National Zoological Park for their explanation of Why Ireland Has No Snakes.

Now snakes are found in deserts, grasslands, forests, mountains, and even oceans virtually everywhere around the world. Everywhere except Ireland, New Zealand, Iceland, Greenland, and Antarctica, that is.

One thing these few snake-less parts of the world have in common is that they are surrounded by water. New Zealand, for instance, split off from Australia and Asia before snakes ever evolved. So far, no serpent has successfully migrated across the open ocean to a new terrestrial home. As the world's oceans have risen and fallen over the millennia, land bridges have come and gone between Ireland, other parts of Great Britain, and the European mainland, allowing animals and early humans to cross. However, any snake that may have slithered it's way to Ireland would have turned into a popsicle when the ice ages hit.

The most recent ice age began about three million years ago and continues into the present. Between warm periods like the current climate, glaciers have advanced and retreated more than 20 times, often completely blanketing Ireland with ice. Snakes, being cold-blooded animals, simply aren't able to survive in areas where the ground is frozen year round. Ireland thawed out for the last time only 15,000 years ago. Since then, 12 miles of icy-cold water in the Northern Channel have separated Ireland from neighboring Scotland, which does harbor a few species of snakes. There are no snakes in Ireland for the simple reason that they can't get there.

[The book cover is from a book by Sheila MacGill Callahan (Author) and Will Hillenbrand (Illustrator). You can buy it on Amazon.com.]