Bacteria respond to stress with more mutation

I’d like to see Mike Behe and Bill Dembski explain this solid research finding.

Carl Zimmer’s new book, Microcosm, has a chapter on E. coli in hostile environments. The bacterium has a precise DNA-repair chemistry (enzyme?) that it uses in normal times. But when it suffers a lot of damage, a fast but sloppy chemistry takes over (different enzyme?). It makes more mistakes but it might keep more bacteria alive.

The result is that in a really hostile environment, e.g. flooded with antibiotics, the bacteria begin to mutate at a rate a hundred times faster than their usual rate. If I read your definition correctly, they increased their evolvability by the same factor. As a result, they evolve at startling rates. That’s probably what happened when bacteria were sent into space and came back with an unexpectedly high number of mutations to help them survive.

When the environment settles down, they go back to using the more precise repair chemistry and the mutation rate falls back to its usual level.

Simply put, it seems to be the bacterial equivalent of panic: When you’re going to die, do something - anything! Maybe it will work.

“Superhumans” at Discovery Channel

The Discovery Channel has a program about people with special abilities.

Feature:

• a woman who tastes sounds
• a man with an extraordinary ability to withstand cold
• a man who can draw in persepective although he’s been blind since birth
• a man who can calculate do rapid mathematical computations
• Ray Kurzweil’s plan to live forever.
• a geneticist who has created cross-species chimeras

The show makes it sound as if we’re directing our own evolution (we’re not). And it’s conflating a bunch of diverse conditions, such as synaesthesia, with evolution rather than neurological cross-wiring. But it is interesting. Follow this link to read these people’s profiles.

Gene Genie #31 at Adaptive Complexity

The 31st edition of Gene Genie has been posted at Adaptive Complexity. See Capitalists, Genetic Tests and Your DNA.

Everyone knows there is a lot of crazy stuff on the internet, but did you know there is a lot of great writing about genes, genetics, and human diseases? And believe it or not, sometimes these pieces are written by people who know what they’re talking about. If you’re looking for what’s new in human genetics, you’ve come to the right place.

Welcome to the 31st Gene Genie, a blog carnival dedicated to great blogging about human genes and how they impact our health. This Mother’s Day edition includes an in-depth highlight of the growing industry of personalized genetics.

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

Here are the earlier Gene Genies:

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

The lovely, sinuous, Gene Genie logo was created by Ricardo at My Biotech Life.

Platypus genome is sequenced

And now we have to put up with newspapers calling the platypus “part bird.” PZ Myers at Pharyngula lets off a little steam in his intro to the platypus genome:

Over and over again, the newspaper lead is that the platypus is “weird” or “odd” or worse, they imply that the animal is a chimera — “the egg-laying critter is a genetic potpourri — part bird, part reptile and part lactating mammal”. No, no, no, a thousand times no; this is the wrong message. … What’s interesting about the platypus is that it belongs to a lineage that separated from ours approximately 166 million years ago, deep in the Mesozoic, and it has independently lost different elements of our last common ancestor, and by comparing bits, we can get a clearer picture of what the Jurassic mammals were like, and what we contemporary mammals have gained and lost genetically over the course of evolution.

Go over and read what the new platypus genome actually tells us about the course of evolution.

Here’s a diagram showing the evolutionary splits. PZ will explain it.

Diagram notes:
Emergence of traits along the mammalian lineage.

• Amniotes split into the sauropsids (leading to birds and reptiles) and synapsids (leading to mammal-like reptiles).
• These small early mammals developed hair, homeothermy and lactation (red lines).
• Monotremes diverged from the therian mammal lineage 166 Myr ago and developed a unique suite of characters (dark-red text).
• Therian mammals with common characters split into marsupials and eutherians around 148 Myr ago (dark-red text).
• Mammal lineages are in red; diapsid reptiles, shown as archosaurs (birds, crocodilians and dinosaurs), are in blue; and lepidosaurs (snakes, lizards and relatives) are in green.
• Geological eras and periods with relative times (Myr ago) are indicated on the left. Myr = “Megayear” or million years.

PZ writes:

This is a fairly conventional picture of our evolutionary history, and I have to emphasize that this paper reinforces the evolutionary explanation for the illustrated relationships.

Scientific logic, executive summary:

if we find a feature in birds that is also present in monotremes, marsupials, or eutherians, it is likely that that feature was also present in our Paleozoic common ancestor….

For instance, one of the unusual (for a mammal) features of the platypus is meroblastic cleavage…. the early [cell] divisions are incomplete — they produce a sheet of cells on top of the large yolk that are cytoplasmically continuous with the yolk cytoplasm…. Birds (archosaurs) and lizards and snakes (lepidosaurs) exhibit meroblastic cleavage. [In contrast, marsupials and eutherians, exhibit complete cleavage from the first division. So] meroblastic cleavage is likely to be a primitive character, one that was inherited from the last common ancestor of synapsids and sauropsids, over 300 million years ago.

Go on and read more: why the platypus isn’t “wierd,” how its venom evolved, what other animals are being sequenced—you know you want to.

U.S. passes Genetic Non-discrimination Act

The U.S. Senate has passed a law which should prevent companies from using people’s personal genetic information to deny them insurance coverage, employment, or other benefits. It’s called GeNA. It need only be signed into law.

I wonder what President Bush will do? In Canada, laws are signed by the Queen’s representative, the Governor General. In theory, the Governor General could refuse to sign a law, but there is a long-standing precedent that he or she will sign any law passed by the House of Commons and Senate, whether or not he, she, or the Queen approves or disapproves of it.

Shake-up at base of the tree of life

New research analysing huge amounts of data suggests that the comb jelly split off from sponges before other multicellular organsisms and went on to develop a nervous system independently of other animals.

(Image from University of California Museum of Paleontology)

You can read about it at Science Daily:

This finding challenges the traditional view of the base of the tree of life, which honored the lowly sponge as the earliest diverging animal. “This was a complete shocker,” says Dunn [no first name given]. “So shocking that we initially thought something had gone very wrong.”

But even after Dunn’s team checked and rechecked their results and added more data to their study, their results still suggested that the comb jelly, which has tissues and a nervous system, split off from other animals before the tissueless, nerveless sponge.

The presence of the relatively complex comb jelly at the base of the tree of life suggests that the first animal was probably more complex than previously believed, says Dunn.

While cautioning that additional studies should be conducted to corroborate his team’s findings, Dunn says that the comb jelly could only have achieved its apparent seniority over the simpler sponge via one of two new evolutionary scenarios:

1. the comb jelly evolved its complexity independently of other animals, after it branched off onto its own evolutionary path; or
2. the sponge evolved its simple form from more complex creatures — a possibility that underscores the fact that “evolution is not necessarily just a march towards increased complexity,” says Dunn. “This scenario would provide a particularly dramatic example of that principle.”

For earlier research on the origin of the nervous system, see “Nervous system originated in sponges.”

Breast is best for babies with the right gene

Breast-feeding boosts children’s IQs by 6 to 7 points over the IQs of kids who weren’t breast-fed, but only if the breast-fed youngsters have inherited a gene variant associated with enhanced biochemical processing of mothers’ milk, reports a team led by psychologist Avshalom Caspi of King’s College London Ninety percent of youngsters possessed the critical FADS2 gene variant. It sounds like non-random natural selection to me.

Forty-seven ways to produce heritable genetic change

Allen MacNeill has taken of the challenge of falsifying the objection to evolution usually framed, “How can random mutation” produce enough variation for evolution?” or “It’s only random mutation and natural selection.” In debate, random mutation is often assumed to be the substitution of one single amino acid for another, in other words, a single point mutation. Allen says,

I promised a list of the real sources of variation that provide the raw material for evolutionary change. It’s taken me a while, but here it is. This list includes “random mutation,’ of course, but also 46 other sources of variation in either the genotypes or phenotypes of living organisms. Note that the list is not necessarily exhaustive, nor are any of the entries in the list necessarily limited to the level of structure or function under which they are listed. On the contrary, this is clearly a list of the minimum sources of variation between individuals in populations. A comprehensive list would almost certainly include hundreds (and possibly thousands) of more detailed processes. Also, the list includes processes that change either genotypes or phenotypes or both, but does not include processes that are combinations of other processes in the list, again implying that a comprehensive listing would be much longer and more detailed.

Here’s his list of forty-six other ways to produce genetic change.

Commenter -DG adds,

Not so much an addition as perhaps a minor correction with the deletions. Not all deletions necessarily result in a frameshift, although of course this would be the most common for deletions of any multiple not of three. But it is certainly possible for 3 (or some multiple of 3) nucleotides to be inserted or deleted at the same time resulting in insertion/deletions of the protein primary sequence. This seems to be especially prevalent in loop regions of the protein three-dimensional structure and may be one of the mechanisms by which new protein domains occasionally arise.

Commenter SPARC adds,

You may add exon shuffling. It belongs to the gene structure section (insertions/deletions) but in most cases the reading frame isn’t changed. I would further add exonization of transposable elements usage of alternate promoters, alternative splicing, multiple polyA signals and trinucleotide repeat expansions.

Commenter Art says,

It would be very nice if you could fold a whole ‘nother universe of genetic and regulatory mechanisms into your list. For the sake of completeness, and because the ID movement (typified by Behe’s recent dismissal of these core mechanisms) cannot deal with the concept.

I speak, of course, of the regulation of gene expression at the level of RNA and protein breakdown. Not only are they central to life (it’s doubtful that multicellular life could exist without the negative regulatory mechanisms afforded by these processes), they are inherently “accessible” to evolutionary modification. This is because, in the ID vernacular, they involve low information modes of recognition and action.

Keywords for a revised list: microRNA, siRNA, exosome, ubiquitin, cullin, E3 ligase, proteasome, SUMO.

Commenter -DG replies,

Great additions SPARC, since I work on protein evolution I really should have remembered to add exon shuffling. Along the same lines of alternative splicing we also have RNA editing. It isn’t carried out in many known systems but its an interesting system as well.

Albino squirrel is seen in Toronto

Albino animals have a genetic inability to produce pigment molecules such as melanin and carotene. As a result, they are wholly or partially white. And they are generally at a disadvantage when it comes to camouflage. Nevertheless, the can survive. (The image at left is an albino squirrel, photographed in the U.S. by Ian Vargas.)

Glendon Mellow at The Flying Trilobite tells us that there’s a white squirrel living in Trinity-Bellwoods Park in Toronto. It’s an albino. Visit his blog for pictures that he took.

According to the Urban Decoder, albino squirrels have been seen around the park since about 1985. Someone else has reported an albino squirrel at Woodbine & Danforth in Toronto. The image at right is a white, non-albino squirrel.

Please look at the Wikipedia entry for “squirrel” for information about colonies of albino squirrels.

Chimp and human DNA

A study in 2006 showed that most of the difference between chimpanzee and human DNA are in regions that don’t code for proteins, but for areas that activate and control other genes.

I’m dubious about this article, because I’m not sure what it means. It starts out,

ScienceDaily (Oct. 13, 2006) — Most of the big differences between human and chimpanzee DNA lie in regions that do not code for genes, according to a new study. Instead, they may contain DNA sequences that control how gene-coding regions are activated and read.

“The differences between chimps and humans are not in our proteins, but in how we use them,” said Katherine Pollard, assistant professor at the UC Davis Genome Center and the Department of Statistics.

Pollard and colleagues at UC Santa Cruz led by David Haussler looked for stretches of DNA that were highly conserved between chimpanzees, mice and rats. Then they compared those sequences to the human genome sequence, to find pieces of DNA that had undergone the most rapid change since the ancestors of chimps and humans diverged about five million years ago.

They found 202 “highly accelerated regions” or HARs, which showed a high rate of evolution between humans and chimps. Only three of those regions contain genes that are likely to encode proteins. The most dramatically accelerated region, HAR1, appears to make a piece of RNA that may have a function in brain development.

DNA, deoxyribonucleic acid, carries the genetic instructions for making a chimp, a human, a tulip or an amoeba. RNA (ribonucleic acid) is an intermediate molecule that transcribes those instructions to make proteins.

The other highly accelerated regions do not appear to code for genes at all, but many are located close to genes involved in controlling when other genes get made, or in growth and development.

“They’re not in genes, but they’re near genes that do some very important stuff,” Pollard said.

Typically, noncoding regions of DNA evolve more rapidly than regions carrying genes, as there is no selective pressure to stop mutations from accumulating. But the human-accelerated regions are highly conserved across the other groups of animals the researchers looked at, suggesting that they do have important functions that stop them from varying too much.

The work is published in the journal Public Library of Science (PLoS) Genetics. A separate paper on HAR1 was published Aug. 17 in the journal Nature. The study was funded by the National Institutes of Health and the Howard Hughes Medical Institute.

Reference: University of California - Davis (2006, October 13). Comparing Chimp, Human DNA. ScienceDaily. Retrieved March 15, 2008, from http://www.sciencedaily.com­ /releases/2006/10/061013104633.htm

Maybe it means exactly what it says, that evolution is taking place in DNA outside genes. Or maybe it means that evolution is taking place in regulatory or activator genes.

The paper in PLOS is here: Forces Shaping the Fastest Evolving Regions in the Human Genome. Tune in on a later post for an analysis.

Mendel’s Garden #24 at BayBlab Blog

The genetics blog carnival, Mendel’s Garden 24 is a BayBlab Blog for March.

Jonathan Wells opens mouth to change feet

On the Panda’s Thumb, Ian Musgrave dissects Jonathan Wells’ arguments against evidence for evolution. He points out Well’s mis-statements about mutations, corrects Wells’s ahistorical garbage about Gregor Mendel; and generally points out that a few minutes of research could find the facts.

For example…
Wells wrote:

Yet Mendel’s theory of genetics contradicted Darwin’s, and Darwinists rejected Mendelian genetics for half a century.

In fact:

While Mendel’s theory of genetics didn’t quite contradict Darwins’s theory of genetics (they were both particulate theories…), it did contradict the most widely held theories of inheritance at the time (blending inheritance…).

Importantly, Mendel’s theory did support Darwin’s theory of natural selection, by showing how variants would not be lost over time (as they were with blending inheritance). Darwinists didn’t reject Mendel’s theory. Mendel’s theory was originally ignored partly because [it was] published in an obscure journal with limited distribution and partly because it attempted a radical mathematical analysis of biology that the few people who read Mendel’s paper did not understand. It was rediscovered by evolutionary biologists in 1900 seeking to understand heredity. Biologists of all stripes rapidly took the theory up….

Mendel’s work was heavily promoted by evolutionary biologists who thought saltation (mutational jumps) drove evolution. The big problem for natural selection was that although Mendelian inheritance explained how favourable traits could persist and not be diluted out, the traits appeared to be binary, you either had a trait or not (incomplete dominance not withstanding). How could it explain traits that appeared to have continuous variation? This was solved between 1918 by statistician RA Fischer and the 30’s by Sewall Wright, JSB Haldane and others, leading to the “Modern synthesis” of the 40’s which fused Darwin’s ideas with population genetics…. Indeed Fischer saw biometry as a way of reconciling the discontinuous nature of Mendelian Inheritance with the continuous variation seen in nature.

Take that, Jonathan Wells!

Ironically, Wells doesn’t even have to resort to research in dusty tomes to find the true value of Gregor Mendel’s work to modern biology. He can search the Web or just buy Simon Mawer’s book, Gregor Mendel: Planting the Seeds of Genetics

A glimpse into bisexuality

PZ Myers at Pharyngula has a long, detailed description of new research into the sexual behavior of fruit flies. It seems that a certain mutation called genderblind, related to the biochemistry of the nervous system, causes male fruit flies to pay equal attention to unresponsive males and females. It’s possible that the mutation makes the nerves more sensitive to stimulation.

The diagram above shows the results of the mutation. A male fly (at the top) is given a choice between a male or female fly. The male is on your left, the female on your right.

• If the decider is an ordinary fly or wild type (”WT”), he chooses the female. His choices are shown as the black bar at the bottom.
• In the middle are the choices by a genderblind (”gb”) fly. You can see that more than half the time he chooses the male fly.

For a glimpse into just what’s going on here, follow the link.

Sandwalk on Calico Cats

Male cats can be black and white or orange and white, and so can female cats; but with the normal number of chromosomes, only female cats are black and orange and white, or “calico.” The reason is that the colour gene for black or orange is on the X chromosome. Males have only one to express. Females are expressing sometimes the X chromosome from their mother and sometimes the X from their father, and thus expressing different colours. The white is caused by another gene that suppresses colour, and can be expressed on more or less of the cat’s hide.

Dilute calico (Peek-A-Boo)

There’s been a discussion on Talk.Origins about calico cats—do they have to be female? The color pattern is an interesting combination of sex-linked genetics and epigenetics. Epigenetics is the inheritance of characteristics other than nuleotide sequence. In this case, it’s inheritance of an inactivated X-chromosome

Go to Larry Moran’s Sandwalk: Calico Cats for a detailed explanation.

The tortoiseshell cat has more blended colours than the calico, but the same sex-linked rules apply. This image from Kittenwars.com is called “Oswald and his sisters.” You can tell which kitten is Oswald because three of the kittens mix orange and black, while one has only black fur—so he’s the male.

I had a long-haired, tortoiseshell cat given to me when she was thirteen years old. She lived for ten more years, making her the oldest cat in my veterinarian’s practice.

Simplified tree of life

From Wikipedia Commons and the Wikipedia article on Evolution, here’s a highly simplifed “tree of life.”