Saturday, February 24, 2007


Hunting Chimpanzees may alter view of Human Evolution (+ Related video)

Reporting findings that help shape our understanding of how tool use has evolved among primates, researchers have discovered evidence that chimpanzees, at least under some conditions, are capable of habitually fashioning and using tools to hunt mammalian prey. The work [1], reported by Jill Pruetz of Iowa State University and Paco Bertolani of the University of Cambridge, will appear online in the journal Current Biology on February 22nd 2007.

Chimpanzees are well known for their ingenuity in using tools for some tasks, such as obtaining invertebrate insects from logs or pounding open hard nuts, but there had been only fleeting evidence of chimpanzees brandishing tools for bona fide hunting.

In the new work, researchers observed tool use in hunting by the Fongoli community of savanna-dwelling chimpanzees (Pan troglodytes verus) in southeastern Senegal. Chimpanzees were observed making spear-like tools in a step-wise fashion, and subsequently using them with jabbing motions in an apparent effort to obtain lesser bushbabies (Galago senegalensis) from cavities in hollow branches or tree trunks. Bushbabies are nocturnal prosimians that retire to such hidden cavities during the day.

Although there was only one successful attempt in 22 recorded instances of the chimpanzees using the spear-like tools to find and obtain prey, the researchers observed that tool-crafting and associated hunting behavior was systematic and consistent, suggesting that it was habitual. The hunting behavior included forceful jabbing motions into branch or trunk hollows, and chimpanzees were seen to subsequently open the hollows by breaking wood off from a distance, suggesting that the jabbing actions were intended to immobilize bushbabies, rather than rouse them from their cavities (bushbabies move quickly and might otherwise easily evade chimpanzees once roused).

Two notable aspects of the behavior observed in the Fongoli group were that on the one hand, it is rare for chimpanzees to consume prosimian prey - in other study sites, red colobus monkeys, hunted mainly by males, are the chimps' most common prey - and on the other hand, the tool use appeared to be primarily restricted to females and immature individuals. These two behavior characteristics could both be related to the fact that the Fongoli community inhabits a mosaic savannah that is relatively dry, and where red colobus monkeys are absent. This habitat may promote efforts - such as the observed tool use - to obtain meat through other means.

The authors point out that the females and immature chimpanzees using the spear-like tools appear to be exploiting a niche relatively ignored by males, an observation that supports a previous hypothesis that female hominids played a role in the evolution of the earliest tool technology and suggests that this technology may have included tools for hunting. [Primatology, Anthropology]

Source: Cell Press / PhysOrg

Info on the Fongoli Savanna Chimpanzee Project (from the National Primate Research Center)


[1] Based on:

Savanna Chimpanzees, Pan troglodytes verus, Hunt with Tools

Jill D. Pruetz and Paco Bertolani

Current Biology: Online Ahead of Issue - Full citation NYA

Although tool use is known to occur in species ranging from naked mole rats [1] to owls [2], chimpanzees are the most accomplished tool users [3, 4, 5]. The modification and use of tools during hunting, however, is still considered to be a uniquely human trait among primates. Here, we report the first account of habitual tool use during vertebrate hunting by nonhumans. At the Fongoli site in Senegal, we observed ten different chimpanzees use tools to hunt prosimian prey in 22 bouts. This includes immature chimpanzees and females, members of age-sex classes not normally characterized by extensive hunting behavior. Chimpanzees made 26 different tools, and we were able to recover and analyze 12 of these. Tool construction entailed up to five steps, including trimming the tool tip to a point. Tools were used in the manner of a spear, rather than a probe or rousing tool. This new information on chimpanzee tool use has important implications for the evolution of tool use and construction for hunting in the earliest hominids, especially given our observations that females and immature chimpanzees exhibited this behavior more frequently than adult males.


Excerpt from Craig Stanford's (Department of Anthropology, University of Southern California) May/June 1995 American Scientist paper "Chimpanzee hunting behavior and human evolution":

In the early 1960s, when the british primatologist Jane Goodall first observed wild chimpanzees hunting and eating meat in Gombe National Park, Tanzania, it was widely believed that these animals were strict vegetarians. Skeptics suggested that the diet of the Gombe chimpanzees was aberrant. Others suggested that the quantity of meat the chimpanzees ate was trivial. After more than 30 years of research, however, it is now clear that meat is a natural part of the chimpanzees' diet. Indeed, hunting has been observed at most of the other sites where chimpanzees are studied across central Africa. And, it turns out, a chimpanzee community may eat several hundred kilograms of meat in a single year.

To many anthropologists this is a surprising development. Of all the higher primates, only human beings and chimpanzees hunt and eat meat on a regular basis. The similarities pose an intriguing prospect: Might the close evolutionary relationship between chimpanzees and human beings provide some clues to the evolution of our own behavior? We do know that the earliest bipedal hominids, the australopithecines, evolved in Africa about 5 million years ago and that they shared a common ancestor with modern chimpanzees shortly before that time. Unfortunately, the evidence for the occurrence of meat-eating among the early australopithecines is spotty at best. Primitive stone tools that were made 2.5 million years ago suggest that early hominids had the means to carve the flesh from large carcasses, but we know very little about their diets before that time. Were they hunters or perhaps, as many anthropologists now argue, scavengers? The behavior of chimpanzees may provide a window through which we can see much that has been lost in the fossil record.

There are also some interesting subtleties to the chimpanzees' hunting behavior that need to be addressed. Although chimpanzees can and do hunt alone, they often form large hunting parties consisting of more than 10 adult males, plus females and juveniles. Chimpanzees also go on "hunting binges" in which they kill a large number of monkeys and other animals over a period of several days or weeks. Such binges have always been a little mysterious. What could incite a chimpanzee to suddenly forgo plant foraging and turn to hunting? Are there social or ecological factors associated with the impetus to hunt? What ecological effects does the chimpanzees' predatory behavior have on their prey?

In the past five years I have been mindful of such questions as I observed the chimpanzees and their primary prey at Gombe, the red colobus monkey. Although we are only beginning to understand some of the causes and consequences of the chimpanzees' actions, what we have discovered is more complicated and more interesting than anyone suspected. For chimpanzees, meat is not only another way to get nutrients like fat and protein, but a means to make political bonds and gain access to sexually receptive females.

Citation 1995 Stanford, C.B. Chimpanzee hunting behavior and human evolution. American Scientist 83 (3): 256-261.

Also see The Bwindi-Impenetrable Great Ape Project


David Attenborough video clip* showing how hunting chimpanzees co-ordinate their behavior in order to trap and kill (then eat) a colobus monkey:

*From The Trials of Life: A Natural History of Behaviour, a BBC nature documentary first broadcast in 1990


The video footage below hasn't any commentary but is accompanied by the following text by kambizkamrani: "Adolescent female Tumbo isolates a potential spear and modifies it. She begins to jab it into a tree to spear her prey. She then climbs the tree and begins jumping on the large limb, which eventually breaks off, allowing her to reach in and retrieve the prey, a bushbaby (Galago senegalensis)." - watching the National Geographic video "Video: Chimps Make and Use 'Spears' to Hunt" first may help.

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What is wrong with intelligent design?

In a thought-provoking paper from the March 2007 issue of The Quarterly Review of Biology , Elliott Sober (University of Wisconsin) clearly discusses the problems with two standard criticisms of intelligent design: that it is unfalsifiable and that the many imperfect adaptations found in nature refute the hypothesis of intelligent design.

Biologists from Charles Darwin to Stephen Jay Gould have advanced this second type of argument. Stephen Jay Gould's well-known example of a trait of this type is the panda's thumb. If a truly intelligent designer were responsible for the panda, Gould argues, it would have provided a more useful tool than the stubby proto-thumb that pandas use to laboriously strip bamboo in order to eat it.

ID proponents have a ready reply to this objection. We do not know whether an intelligent designer intended for pandas to be able to efficiently strip bamboo. The "no designer worth his salt" argument assumes the designer would want pandas to have better eating implements, but the objection has no justification for this assumption. In addition, Sober points out, this criticism of ID also concedes that creationism is testable.

A second common criticism of ID is that it is untestable. To develop this point, scientists often turn to the philosopher Karl Popper's idea of falsifiability. According to Popper, a scientific statement must allow the possibility of an observation that would disprove it. For example, the statement "all swans are white" is falsifiable, since observing even one swan that isn't white would disprove it. Sober points out that this criterion entails that many ID statements are falsifiable; for example, the statement that an intelligent designer created the vertebrate eye entails that vertebrates have eyes, which is an observation.

This leads Sober to jettison the concept of falsifiability and to provide a different account of testability. "If ID is to be tested," he says, "it must be tested against one or more competing hypotheses." If the ID claim about the vertebrate eye is to be tested against the hypothesis that the vertebrate eye evolved by Darwinian processes, the question is whether there is an observation that can discriminate between the two. The observation that vertebrates have eyes cannot do this.

Sober also points out that criticism of a competing theory, such as evolution, is not in-and-of-itself a test of ID. Proponents of ID must construct a theory that makes its own predictions in order for the theory to be testable. To contend that evolutionary processes cannot produce "irreducibly complex" adaptations merely changes the subject, Sober argues.

"When scientific theories compete with each other, the usual pattern is that independently attested auxiliary propositions allow the theories to make predictions that disagree with each other," Sober writes. "No such auxiliary propositions allow … ID to do this." In developing this idea, Sober makes use of ideas that the French philosopher Pierre Duhem developed in connection with physical theories - theories usually do not, all by themselves, make testable predictions. Rather, they do so only when supplemented with auxiliary information. For example, the laws of optics do not, by themselves, predict when eclipses will occur; they do so when independently justified claims about the positions of the earth, moon, and sun are taken into account.

Similarly, ID claims make predictions when they are supplemented by auxiliary claims. The problem is that these auxiliary assumptions about the putative designer's goals and abilities are not independently justified. Surprisingly, this is a point that several ID proponents concede.

Source: University of Chicago Press Journals /Eureka Alert


Related paper:

What is Wrong with Intelligent Design?

Elliott Sober

The Quarterly Review of Biology, March 2007, Vol. 82, No. 1
Copyright 2007 by The University of Chicago. All rights reserved.

This article reviews two standard criticisms of creationism/intelligent design (ID): it is unfalsifiable, and it is refuted by the many imperfect adaptations found in nature. Problems with both criticisms are discussed. A conception of testability is described that avoids the defects in Karl Popper's falsifiability criterion. Although ID comes in multiple forms, which call for different criticisms, it emerges that ID fails to constitute a serious alternative to evolutionary theory.


Science Friday (Audio) for February 23, 2007, Hour Two:

In this hour of Science Friday, we'll look at a collection of topics centered around evolution, creationism, and education. First, we'll take a look back at the Dover, Pennsylvania evolution trial. The judge's (John E. Jones III) ruling in that case dealt a blow to one district's plans to bring "intelligent design" to its public school science classes. We'll talk with the Pulitzer Prize winning author (Edward Humes) of a new book on the trial.

We'll also talk with the director (Randy Olson) of "A Flock of Dodos," a new film that tackles the question of why scientists can't seem to get the intelligent design debate to go away. Plus, an update on the nationwide battle over teaching creationism in public schools. Did the fall elections bring any changes to policies in science education battlegrounds such as Kansas?

Other Guest: Nick Matzke, Public Information Project Director, National Center for Science Education


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Thursday, February 22, 2007


Lizards 'Shout' Against a Noisy Background Discovery

Lizards that signal to rivals with a visual display "shout" to get their point across, UC Davis researchers have found.

Male anole lizards signal ownership of their territory by sitting up on a tree trunk, bobbing their heads up and down and extending a colorful throat pouch (dewlap). They can spot a rival lizard up to 25 meters away, said Terry Ord, a postdoctoral researcher at UC Davis who is working with Judy Stamps, professor of evolution and ecology.

The lizards' signals need to be strong enough for a rival to see, but not vivid enough to say "eat me" to a passing predator. But their forest home can be a visually noisy environment, with branches and leaves waving in the breeze and casting patterns of light and shade.

"They have to have a strategy to get their message across," Ord said.

Anolis lineatopus Jamaican grey/crested anole, Discovery Bay, Jamaica

Image: Postdoctoral researcher Terry Ord says anole lizards, such as this one, create a strategy to get their message across to rivals. (Courtesy photo UCD)

Ord videotaped two species of anole lizards, Anolis cristatellus and Anolis gundlachi, in the Caribbean National Forest in Puerto Rico. He found that the more "visual noise" in the background, the faster and more exaggerated the movements of the lizards.

Anole lizards are interesting to evolutionary biologists because different species are found on different islands all over the Caribbean. The lizards are not particularly closely related - they are separated by 30 million years of evolution - but they live in similar environments with the same obstacles to communication. So Ord is using them as a model to investigate the evolution of such signals.

The other authors on the paper, which is published online in Proceedings of the Royal Society part B, are Richard A. Peters, Australian National University, Canberra; and Barbara Clucas, a graduate student in animal behavior at UC Davis. The work was supported by grants from the National Geographic Society, the National Science Foundation and the Australian Research Council.

Source: University of California Davis PR February 21, 2007


Lizards speed up visual displays in noisy motion habitats

Terry J. Ord, Richard A. Peters, Barbara Clucas, Judy A. Stamps

Proceedings of the Royal Society B: Biological Sciences
ISSN: 0962-8452 (Paper) 1471-2954 (Online)
Issue: FirstCite Early Online Publishing
DOI: 10.1098/rspb.2006.0263

Extensive research over the last few decades has revealed that many acoustically communicating animals compensate for the masking effect of background noise by changing the structure of their signals. Familiar examples include birds using acoustic properties that enhance the transmission of vocalizations in noisy habitats. Here, we show that the effects of background noise on communication signals are not limited to the acoustic modality, and that visual noise from windblown vegetation has an equally important influence on the production of dynamic visual displays. We found that two species of Puerto Rican lizard, Anolis cristatellus and A. gundlachi, increase the speed of body movements used in territorial signalling to apparently improve communication in visually 'noisy' environments of rapidly moving vegetation. This is the first evidence that animals change how they produce dynamic visual signals when communicating in noisy motion habitats. Taken together with previous work on acoustic communication, our results show that animals with very different sensory ecologies can face similar environmental constraints and adopt remarkably similar strategies to overcome these constraints.

The above paper references:

Evolution of Anoline Lizard Display Behavior

Thomas A Jennsen

American Zoologist* 1977 17(1):203-215; doi:10.1093/icb/17.1.203

Based on my conceptual framework of anoline display behavior, I am suggesting the following evolutionary trends. Lateral presentation during display was probably promoted by monocular vision. Along with lateral presentation, postures evolved to increase lateral outline. These postures which magnified body size were probably of selective advantage within aggressive social contexts since larger animals tend to dominate smaller ones through bluff. Body movement evolved along with lateral orientation and size-enhancing postures. These movements would be most effective if they complemented lateral orientation. Effectors available for such movements were primarily pre-adapted for vertical motion. The patterns of movement generated were probably simple oscillatory bobbing movements by the head which were weakly stereotyped, interspecifically similar, appearing in many contexts, and having a weakly defined information content. Events having selective advantage for species recognition promoted stereotypy of bobbing behavior into species-unique displays; each species had its unique signature display which served in a manifold communicatory capacity. The signature display appeared in assertion, courtship, and challenge contexts. Its information content varied depending upon context and recipient of the display (e.g., male or female). Besides the stereotyped aspects of the display, certain features remained variable with potential information significance. Core variability (see text) promotes individual recognition and may be the origin of new unique display patterns as sibling species emerge. Display modifiers (see text) are variable display features shared by members of a population (many being shared interspecifically) that provide a graded appearance to display performance; modifiers can indicate level of arousal and facilitate interspecific communication. For some species display repertoire size seems to have evolved from a single display (signature display) to repertoires of multiple displays; these subsequent displays are generally restricted to aggressive interactions.

*American Zoologist is now Integrative and Comparative Biology


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Wednesday, February 21, 2007


An ancient retrovirus is resurrected

Retroviruses have been around longer than humanity itself. In fact, the best-known family member, HIV, is a relative youngster, with its first known human infections occurring sometime in the mid-20th century. But although many retroviruses went extinct hundreds of thousands or millions of years ago, researchers studying the pathogens don't use the traditional tools of paleontologists: They need look only as far as our own DNA. Retroviruses infect cells and replicate by inserting their DNA into their host cell's genome. If that cell happens to be a germ cell, such as a sperm, an egg or their precursors, then the retroviral DNA is inherited by offspring just like a normal gene. Humans have many defunct retroviruses deposited in our DNA, remnants of ancient retroviruses that replicated in our ancestors millions of years ago. Now, researchers have brought one of those retroviruses back to life.

"In our DNA, there's a fossil record of retroviruses that used to infect us," says Paul Bieniasz, associate professor and head of the Laboratory of Retrovirology at Rockefeller University and the Aaron Diamond AIDS Research Center [Aids]. In fact, about eight percent of human DNA is made up of retroviral sequences. Bieniasz and Youngnam Lee, a graduate student in the Bieniasz lab, have excavated some of that DNA and - in an attempt to better understand how humans and retroviruses co-evolved - they have resurrected an ancient retrovirus, one that can create new viral particles and infect human cells. They describe their work in a paper published by PLoS Pathogens last month [1].

The extinct retroviruses embedded in our DNA can't reproduce because of mutations in one or more of their genes. The younger of these human endogenous retroviruses (or HERVs) have fewer changes, and judging by the paucity of genetic alterations, at least one subfamily - HERV-K - was likely still active less than a few hundred thousand years ago. Different members of this subfamily have slightly different mutations. "But as of a few months ago," Bieniasz says, "there was no replication-competent form of this virus."

To eliminate those mutations that kept HERV-K from replicating, the two researchers deduced a genetic sequence that was a consensus of 10 different HERV-K proviruses (provirus) and synthesized the whole viral genome from scratch. Then, they took that sequence (which they dubbed HERV-KCON) and inserted it into cultured human cells to see if it would result in the creation of HERV-K structural proteins. Their consensus sequence resulted in not only functional proteins, but in a retrovirus that was capable of creating new viral particles and integrating itself into a host cell's genome. "This is the first time this has been done with a viral genome that was effectively dead, and now is alive - or at least has all the functions that suggest it should replicate," Bieniasz says.

The project began, Lee says, because certain human and non-human primate cells produce proteins that appear to block HIV from replicating. "And the question is where did the proteins come from?" she asks. "By studying these extremely old viruses, we can tap into what happened in our ancestors millions and millions of years ago."

Source: Rockefeller University PR February 20, 2007


[1] Reconstitution of an Infectious Human Endogenous Retrovirus

Young Nam Lee and Paul D. Bieniasz

Citation: Lee YN, Bieniasz PD (2007) Reconstitution of an Infectious Human Endogenous Retrovirus. PLoS Pathogens 3(1): e10 doi:10.1371/journal.ppat.0030010


Authors Summary

Retrovirus genomes integrate into the genomes of host cells. If the target cells of a particular retrovirus include germ-line cells, e.g., sperm or egg cells, then retroviral genomes can be inherited like cellular genes. So-called endogenous retroviruses have accumulated throughout evolution in the genomes of many organisms, including humans. While all known endogenous retroviruses of modern humans are unable to replicate as retroviruses, the human genome represents a fossil record of ancient retroviruses that once infected our ancestors. In this study, a collection of "dead" endogenous retroviral genomes in modern human DNA was used to deduce the approximate sequence of an ancestral retrovirus, human endogenous retrovirus (HERV)-K, that is now thought to be extinct. A pseudo-ancestral HERV-K DNA sequence was synthesized and used to produce viral proteins and RNA that could reconstitute the HERV-K replication cycle. Thus, the replication and biology of a once-extinct retrovirus can now be studied in the laboratory. Interestingly, reconstituted HERV-K replication experiments, and comparison of the reconstituted HERV-K DNA sequence with the dead HERV-Ks in modern human DNA, suggests that HERV-K may have been extinguished in humans in part by host defenses that induce mutation of retroviral DNA and that the reconstitution of the pseudo-ancestral HERV-K reversed these changes.


The human genome represents a fossil record of ancient retroviruses that once replicated in the ancestors of contemporary humans. Indeed, approximately 8% of human DNA is composed of sequences that are recognizably retroviral. Despite occasional reports associating human endogenous retrovirus (HERV) expression with human disease, almost all HERV genomes contain obviously inactivating mutations, and none are thought to be capable of replication. Nonetheless, one family of HERVs, namely HERV-K(HML-2), may have replicated in human ancestors less than 1 million years ago. By deriving a consensus sequence, we reconstructed a proviral clone (HERV-KCON) that likely resembles the progenitor of HERV-K(HML-2) variants that entered the human genome within the last few million years. We show that HERV-KCON Gag and protease proteins mediate efficient assembly and processing into retrovirus-like particles. Moreover, reporter genes inserted into the HERV-KCON genome and packaged into HERV-K particles are capable of infectious transfer and stable integration in a manner that requires reverse transcription. Additionally, we show that HERV-KCON Env is capable of pseudotyping HIV-1 particles and mediating entry into human and nonhuman cell lines. Furthermore, we show that HERV-KCON is resistant to inhibition by the human retrovirus restriction factors tripartite motif 5alpha and apolipoprotein B mRNA-editing enzyme, catalytic polypeptide-like (APOBEC) 3G but is inhibited by APOBEC 3F. Overall, the resurrection of this extinct infectious agent in a functional form from molecular fossils should enable studies of the molecular virology and pathogenic potential of this ancient human retrovirus.


A characteristic that is unique to retroviruses is their propensity to integrate their genomes into host-cell DNA as an essential part of their replication cycle. Thus, if the target cell population of a given retrovirus includes germ cells or their progenitors, retroviral genomes can be inherited in a Mendelian manner as so-called "endogenous" forms (see [1] for review). Indeed, endogenous retroviruses have accumulated over time in the genomes of many organisms and are extraordinarily common in mammals, comprising approximately 8% of human DNA [2]. Nonetheless, while some avian, murine, and primate species harbor replication-competent retroviruses within their genomes, intact retroviruses are relatively infrequent and almost all endogenous retroviruses are obviously defective due to the presence of stop codons and frameshifts in one or more genes.

Among the numerous families of defective human endogenous retroviruses (HERVs) found in modern human DNA, the human mouse mammary tumor virus-like 2 (HML-2) subfamily of HERV-K proviruses is of special interest. Even though replication-competent forms of HERV-K(HML-2) have not been found, some proviruses were deposited in the human genome after speciation and represent some of the youngest HERVs known [3-6]. Also, occasional reports link their expression with human disease [7]. The age of an endogenous provirus can be roughly estimated by comparing sequence of the two long terminal repeats (LTRs). At integration, the two proviral LTRs should be identical, but during host DNA replication, each LTR independently accumulates mutations as a function of age, and it is estimated that one difference between two LTRs should occur every approximately 200,000 to 450,000 y. Several HERV-K(HML-2) proviruses have been identified in human DNA that have less than five differences between the two LTRs, suggesting deposition perhaps less than 1 million y ago [3-6]. HERV-K(HML-2)-related proviruses are found only in Old World primates genomes, and many are unique to humans, with nonhuman primate genomes containing empty preintegration sites at orthologous loci. Compellingly, polymorphism exists in humans with respect to the presence or absence of proviruses at some HERV-K integration sites, indicating insertion relatively recently in human evolution [3-6]. Furthermore, many of the younger HERV-K(HML-2) proviruses contain a subset of open reading frames (ORFs) with a few or no mutations [3,6,8]. However, all known HERV-K proviruses are replication defective.

There are several ways in which a defective provirus can proliferate in a host's genome, including via exogenous infection events following complementation in trans, where functional proteins are supplied by other endogenous or exogenous viruses. Alternatively, for some retroelements, envelope-independent retrotransposition can occur in cis, where an element copies itself and inserts into a new genomic locus within the same cell, forgoing the normal extracellular phase of the retroviral life cycle. Defective proviruses can also be proliferated as a result of long interspersed element retrotransposition [9]. However, most HERV-K(HML-2) replication appears to have been a consequence of autonomous infection by extracellular virions [10,11]. This conclusion is based on the comparatively low number of stop codons and ratio of nonsynonymous to synonymous changes (dN/dS) in HERV-K ORFs, indicating a purifying selection on all proteins. Notably, this finding holds for HERV-K Env [10], which should be required for replication that includes an extracellular step but not for any other mode of provirus proliferation.

Ancient retroviruses are of interest, in part because they likely imposed selective pressure on host defenses in human ancestors. Indeed, the tripartite motif (TRIM) 5alpha and apolipoprotein B mRNA-editing enzyme, catalytic polypeptide-like (APOBEC) 3 proteins that provide part of the host defense against modern retroviruses have been under positive selection for much of primate evolution [12-16]. As a retrovirus that appears to have replicated in the ancestors of modern Old World monkeys, apes, and humans, HERV-K may be partly responsible for this pressure. Moreover, it is conceivable that HERV-K exists today in an undetected replication-competent form in rare humans [4]. However, no studies of the virology or pathogenic potential of this ancient human virus have been possible because a contemporary, replication-competent HERV-K strain has not been identified and may not exist at all.

Despite some functional degradation due to mutation during deposition or during human DNA replication, HERV-K(HML-2) proviruses that have been deposited in human DNA in the past few million years should be reasonably well preserved and have relatively few inactivating mutations. Indeed, various studies have shown that individual proteins from certain HERV-K proviruses can function in vitro [17-25]. We reasoned that it might be possible to resurrect HERV-K(HML-2) in replication-competent form using proviruses that are thought to have most recently entered the human genome as a template. Therefore, we constructed a HERV-K strain whose genome sequence is a consensus of a subset of HERV-K(HML-2) proviruses. Importantly, we demonstrate that all viral proteins necessary for viral replication encoded by this provirus are functional and that proteins and genomes based on the reconstructed HERV-K(HML-2) viral genome can be used to generate infectious exogenous retrovirus particles.


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Tuesday, February 20, 2007


Studies of population genetics, evolution are an exercise in bad taste

Scientific studies of why foods such as Brussels sprouts and stout beer are horribly bitter-tasting to some people but palatable to others are shedding light on a number of questions, from the mechanisms of natural selection to understanding how our genes affect our dietary habits (see "Origins and Evolution of Human Diet").

Dr. Stephen Wooding, a population geneticist at UT Southwestern Medical Center in Dallas, studies how slight variations in genes give rise to variations in traits among a given human population.

Part of Dr. Wooding's research focuses on variations in the genes responsible for bitter-taste receptors, tiny receptacles on the tongue that intercept harsh-tasting chemicals from food. Each of these genes comes in several forms, and the forms you carry help determine how you perceive bitter-tasting compounds.

The ability to taste or not taste bitter foods might have played a role in human evolution and may today account for such health-related behaviors as smoking and vegetable consumption, Dr. Wooding said. He presented an overview of his research on the bitter-taste receptor in San Francisco at the 2007 annual meeting of the American Association for the Advancement of Science (AAAS). The title of his talk is "Evolution: A Study in Bad Taste?" [1]

In the 1930s, scientists discovered differences in the ability of humans to taste a bitter synthetic compound called phenylthiocarbamide, or PTC, and they determined that the trait was controlled by genetics (the actual gene for PTC sensitivity was discovered in 2003). For PTC "tasters," even tiny concentrations of the compound are extremely bitter, while "nontasters" experience little or no taste to the same concentration of PTC.

"In some ways, bitter-taste sensitivity seems to be a trivial trait, but early geneticists recognized that this trait was special, for a variety of reasons," said Dr. Wooding, an assistant professor with UT Southwestern's Eugene McDermott Center for Human Growth and Development.

"Bitter-taste sensitivity is crucially important in protecting the human body from toxins in the environment. By enabling us to perceive noxious chemicals in potential foods - especially toxins used by plants to defend themselves against herbivores - bitter taste probably helped our early ancestors avoid poisoning," he said.

If that is the case, then why are both tasters and nontasters still present in the human population? Based on the rules of natural selection, shouldn't all of the nontasters have died off early in our evolution?

The answer is complex, Dr. Wooding said, noting that some things that taste bitter are used as medicine, such as compounds in certain tree barks that help protect against malaria.

He and his colleagues - Drs. Dennis Drayna and Un-kyung Kim at the National Institutes of Health, along with Drs. Lynn Jorde and Michael Barnshad at the University of Utah - analyzed the gene for PTC sensitivity for certain "signatures" of natural selection that would tell them how the gene has changed over time. They found very strong evidence that within humans, a process called "balancing natural selection" has taken place.

"This is a kind of natural selection that keeps two different forms of the same gene active in a population," Dr. Wooding said. "In this case they are the taster and the nontaster forms. In the absence of this type of natural selection, you would expect one form to dominate. That hasn't happened here because for some reason, there is not a strong advantage of one over the other. It's an unusual situation."

One hypothesis is that PTC nontasters can taste something that tasters can't.

"When we look at the nontaster form of the PTC receptor, it looks functional, so we think it probably responds to something," Dr. Wooding said. "One explanation could be that, long ago, it conferred some sort of protection from a different compound in these people."

Follow-up studies of variation in other bitter-taste receptor genes have revealed that different genes show different patterns of diversity. These might match up with other person-to-person differences in taste, Dr. Wooding said.

Regardless of the form of the PTC gene an individual carries, Dr. Wooding - who genetically is a taster - emphasized that taste preferences, upbringing and cultural issues clearly play very important roles in a person's diet.

"I personally like a little bit of bitter taste," he said.

Source (Adapted): University of Texas Southwestern Medical Center February 16, 2007


[1] See the 2005 Current Biology paper:

Evolution: A Study in Bad Taste?

Stephen Wooding

Current Biology Volume 15, Issue 19, 11 October 2005, Pages R805-R807


Bitter tastes are among the most salient of life's experiences - who can forget one's first encounter with dandelion milk or a stout beer? Studies of the genes underlying these tastes are providing new perspectives on human origins and health.


Bitter-taste sensitivity, of course, begins on the tongue. Concentrated at the back of the tongue, on disc-like structures called circumvallate papillae, specialized bitter-taste receptor cells await contact with potentially bitter compounds. Upon exposure to an appropriate ligand, these receptor cells depolarize, generating a signal that is conveyed via the facial and glossopharyngeal nerves to the brain (Figure 1A). In principle, any mechanism that stimulates this neural pathway will lead to the sensation of bitter taste; however, recent studies have highlighted the importance of a small group of G-protein-coupled receptors encoded by the TAS2R (also called T2R) gene family.

In humans, this family includes roughly 25 functional genes and eight pseudogenes, each roughly a kilobase in length, found in three clusters on chromosomes 5, 7 and 12. The protein products of these genes are concentrated at the apex of bitter-taste receptor cells, near the taste pore, where they are positioned to bind bitter ligands as they wash past, dissolved in saliva (Figure 1A). Upon ligand binding, these receptors catalyze a series of reactions leading to the efflux of intracellular calcium, and the cascade of events leading to taste perception begins (Figure 1B).


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Monday, February 19, 2007


Michigan Researcher Hopes to Unlock Evolutionary Secrets

Roughly 2 1/2 billion years ago, some algae began to photosynthesize, an astonishing development that led to the creation of plants and a myriad of complex life forms, including, incidentally, mankind.

Today, Eric Linton, a Central Michigan University assistant professor of biology, is studying the gene makeup of single-celled euglenoids - single-celled organisms that acquired the ability to photosynthesize from algae - to learn whether that evolutionary step was a single hallmark moment or a series of events over time.

Eventually, Linton hopes to learn whether dormant genes that once controlled photosynthesis in certain euglenoids can reactivate, shedding light on whether scientists can jumpstart long-dormant genes in other organisms, such as in humans to fight a host of diseases.

With a 354,000 dollar grant from the National Science Foundation, Linton has begun a three-year project to perform complete genome sequencing of six forms of euglenoids, some of which long ago lost the ability to photosynthesize.

A focus of Linton's research is chloroplasts - components of euglenoid cells that serve as an engine for photosynthesis, or the synthesis of sugar from light, carbon dioxide and water. Some of the euglenoids under study have functioning chloroplasts, enabling photosynthesis; in others, the chloroplasts apparently are dormant.

By examining the genes for chloroplasts from six different euglenoids, Linton hopes to learn whether all acquired the ability to photosynthesize from the same ancestor, or multiple ancestors. Also, Linton wants to deduce how the genes are transferred, lost or evolved when two genomes are combined.

The discovery of supposedly dormant genes in the euglenoids raises questions about whether such genes - both in euglenoids and humans - can receive a man-made jump-start one day.

"If they are keeping these genes around," Linton said, "they must be achieving something."

Most genome sequencing will occur off-campus, but Linton plans on using a 50,000 dollar differential interference contrast microscope - which provides near 3D imaging - for much of the study. A graduate student and two undergraduates will assist him.

Linton, who joined CMU in July 2006, earned his doctorate in 2000 from Rutgers University in New Jersey.

Source: Central Michigan University PR January 31, 2007


An earlier paper co-authored by Eric Linton:

Pattern of diversity in the genomic region near the maize domestication gene tb1

Richard M. Clark, Eric Linton, Joachim Messing, and John F. Doebley

PNAS | January 20, 2004 | vol. 101 | no. 3 | 700-707

Domesticated maize and its wild ancestor (teosinte) differ strikingly in morphology and afford an opportunity to examine the connection between strong selection and diversity in a major crop species. The tb1 gene largely controls the increase in apical dominance in maize relative to teosinte, and a region of the tb1 locus 5' to the transcript sequence was a target of selection during maize domestication. To better characterize the impact of selection at a major "domestication" locus, we have sequenced the upstream tb1 genomic region and systematically sampled nucleotide diversity for sites located as far as 163 kb upstream to tb1. Our analyses define a selective sweep of {approx}60-90 kb 5' to the tb1 transcribed sequence. The selected region harbors a mixture of unique sequences and large repetitive elements, but it contains no predicted genes. Diversity at the nearest 5' gene to tb1 is typical of that for neutral maize loci, indicating that selection at tb1 has had a minimal impact on the surrounding chromosomal region. Our data also show low intergenic linkage disequilibrium in the region and suggest that selection has had a minor role in shaping the pattern of linkage disequilibrium that is observed. Finally, our data raise the possibility that maize-like tb1 haplotypes are present in extant teosinte populations, and our findings also suggest a model of tb1 gene regulation that differs from traditional views of how plant gene expression is controlled.


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Sunday, February 18, 2007


Out of Africa - Bacteria, as well (Helicobacter pylori)

When man made his way out of Africa some 60,000 years ago to populate the world, he was not alone: He was accompanied by the bacterium Helicobacter pylori, which causes gastritis in many people today. Together, man and the bacterium spread throughout the entire world. This is the conclusion reached by an international team of scientists led by Mark Achtman from the Max Planck Institute for Infection Biology in Berlin, Germany. The researchers also discovered that differences developed in the genetic makeup of the bacteria populations, just as it did in that of the various peoples of the world. This has also given scientists new insight into the paths taken by man as he journeyed across the Earth.

Migration paths of Modern Man and the bacterium Helicobacter pylori

The migration paths taken by modern man as he colonized the world. 60,000 years ago, Homo sapiens left his original home in East Africa - taking the bacterium Helicobacter pylori with him. The abbreviation kyears stands for thousand years. Image: Max Planck Institute for Infection Biology

More than half of all human beings are infected with Helicobacter pylori, a bacterium that can cause stomach ulcers. Like humans, the bacteria are also split up into numerous regional populations. A team of scientists led by Mark Achtman at the Max Planck Institute for Infection Biology, François Balloux at the University of Cambridge and Sebastian Suerbaum at Hanover Medical University have found signs of the parallel evolution of man and H. pylori. Using mathematical simulations, the researchers demonstrated that H. pylori must have left East Africa at the same time as man - around 60,000 years ago. This astonishing conformity was uncovered by scientists when they compared the nucleotide sequencing patterns in the DNA of human and H. pylori populations.

In order to characterise the individual populations, the scientists employed the principle of isolation by distance. According to this principle, the genetic distance between two populations has a linear correlation with the length of the migration paths taken since they were separated. "It's actually quite logical," explains Dr. Mark Achtman, "because in the time that elapses after a population leaves its point of origin, the number of mutations in its genetic makeup continually increases."

However, while man was spreading throughout the world, human populations had to repeatedly pass through what scientists call genetic bottlenecks: when a population shrinks, the gene pool also becomes smaller. These losses in genetic diversity linger, even when the population starts once again to increase in number. Since the Homo sapiens populations usually had to pass through several genetic bottlenecks on their way across the globe, their genetic diversity declined the further they journeyed from their origin in East Africa.

Scientists have now uncovered similar signs of historical population migration in the genetic makeup of H. pylori. However, the genetic diversity of the bacteria is larger than that of man. This paves the way for researchers to use H. pylori data to work out the migratory movements of modern man. "The parallels between the spread of man and of H. pylori are truly astonishing," says Achtman. "This bacterium could help us attain further information on aspects of human history that are still hotly disputed today if we analyzed H. pylori in conjunction with human data." For example, after leaving East Africa, the H. pylori population spread through limited localities in southern Africa, West Africa, Northeast Africa, India and East Asia. The genes of bacteria isolated in Europe, for instance, reveal influences from Central Asia - an indication that human immigrants came to Europe from Asia.

Source: Max Planck Society PR "Out of Africa - Bacteria, as well" News B / 2007 (14) February 14th, 2007


Based on:

An African origin for the intimate association between humans and Helicobacter pylori

Bodo Linz, François Balloux, Yoshan Moodley, Andrea Manica, Hua Liu, Philippe Roumagnac, Daniel Falush, Christiana Stamer, Franck Prugnolle, Schalk W. van der Merwe, Yoshio Yamaoka, David Y. Graham, Emilio Perez-Trallero, Torkel Wadstrom, Sebastian Suerbaum and Mark Achtman

Nature advance online publication 7 February 2007 | doi:10.1038/nature05562; Received 4 October 2006; Accepted 22 December 2006; Published online 7 February 2007

Infection of the stomach by Helicobacter pylori is ubiquitous among humans. However, although H. pylori strains from different geographic areas are associated with clear phylogeographic differentiation, the age of an association between these bacteria with humans remains highly controversial. Here we show, using sequences from a large data set of bacterial strains that, as in humans, genetic diversity in H. pylori decreases with geographic distance from east Africa, the cradle of modern humans. We also observe similar clines of genetic isolation by distance (IBD) for both H. pylori and its human host at a worldwide scale. Like humans, simulations indicate that H. pylori seems to have spread from east Africa around 58,000 yr ago. Even at more restricted geographic scales, where IBD tends to become blurred, principal component clines in H. pylori from Europe strongly resemble the classical clines for Europeans described by Cavalli-Sforza and colleagues. Taken together, our results establish that anatomically modern humans were already infected by H. pylori before their migrations from Africa and demonstrate that H. pylori has remained intimately associated with their human host populations ever since.


Related papers:

The co-evolved Helicobacter pylori and gastric cancer: trinity of bacterial virulence, host susceptibility and lifestyle
Yusuf Akhter, Irshad Ahmed, S Manjulata Devi and Niyaz Ahmed

Infectious Agents and Cancer 2007, 2:2


Helicobacter pylori is an important yet unproven etiological agent of gastric cancer. H. pylori infection is more prevalent in developing Asian countries like India and it is usually acquired at an early age. It has been two decades since Marshall and Warren (1984) first described curved bacilli in the stomach of ulcer and gastritis patients. This discovery has won them the Nobel Prize recently [2], but the debate whether H. pylori is a pathogen or a commensal organism is still hot. Associations with disease-specific factors remain illusive years after the genome sequences were made available. Cytotoxin-associated antigen A (CagA) and the so-called plasticity region cluster genes are implicated in pathogenesis of the carcinoma of stomach. Another virulence factor VacA whose role is still debatable, has recently been projected in pathology of gastric cancer. Studies of the evolution through genetic variation in H. pylori populations have provided a window into the history of human population migrations and a possible co-evolution of this pathogen with its human host. Possible symbiotic relationships were seriously debated since the discovery of this pathogen. The debate has been further intensified as some studies proposed H. pylori infection to be beneficial in some humans. In this commentary, we attempt to briefly discuss about H. pylori as a human pathogen, and some of the important issues linked to its pathophysiology in different hosts.

'We dance around in a ring and suppose, the secret sits in the middle and knows' - Robert Frost

[2] Barry J. Marshall and J. Robin Warren won the 2005 Nobel Prize in Physiology or Medicine


Evolution of the Helicobacter pylori Vacuolating Cytotoxin in a Human Stomach

Francisco Aviles-Jimenez, Darren P. Letley, Gerardo Gonzalez-Valencia, Nina Salama, Javier Torres, and John C. Atherton

J Bacteriol. 2004 August; 186(15): 5182-5185.
doi: 10.1128/JB.186.15.5182-5185.2004.
Copyright 2004, American Society for Microbiology


We describe two subclones of Helicobacter pylori, isolated contemporaneously from a human stomach, which differ markedly in the vacuolating cytotoxin gene, vacA, but whose near identity in sequences outside this locus implies a very recent common origin. The differences are consistent with homologous recombination with DNA from another strain and result in a changed vacA midregion and, importantly, in changed toxicity.


We have shown that the VacA toxin can evolve in vivo to alter its toxicity, presumably through recombination with another, unidentified, H. pylori strain. Because only two strains were identified, we cannot be certain which is the daughter, but both acquisition and loss of toxin activity within the stomach have important potential implications for pathogenesis and future clinical management strategies. For example, if H. pylori pathogenicity changes, disease expression may change, conceivably contributing to phenomena such as the waxing and waning of ulcers. One reason for developing typing systems for H. pylori based on virulence determinants such as vacA has been the hope that such strains could be identified and treated before they cause disease. If rapid evolution in vivo as demonstrated here is widespread, such a strategy would be illogical. One challenge now is to assess whether the evolution of virulence determinants such as vacA and cag is a common phenomenon, as would be predicted from the observed extent and pattern of DNA sequence diversity at other loci . That it has been demonstrated by chance in vacA in this study and in cag in a previous study would imply that such evolution is not rare.


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