Showing posts with label Evolution. Show all posts
Showing posts with label Evolution. Show all posts
Monday, February 23, 2009
Friday, March 28, 2008
Quote of the Day
"The other thing we evolutionary biologists don't do enough of, and this stems from the previous point, is make an emotional and moral case for the study of evolution. Last night, I concluded my talk with a quote from Dover, PA creationist school board member William Cunningham, who declared, "Two thousand years ago someone died on a cross. Can't someone take a stand for him?"
My response was, "In the last two minutes, someone died from a bacterial infection. We take a stand for him.""
From: http://scienceblogs.com/mikethemadbiologist/2008/03/another_fight_about_framing_an.php
Simple, and concise.
My response was, "In the last two minutes, someone died from a bacterial infection. We take a stand for him.""
From: http://scienceblogs.com/mikethemadbiologist/2008/03/another_fight_about_framing_an.php
Simple, and concise.
Monday, August 13, 2007
Thursday, June 14, 2007
The Monster in the Closet...
The experiment, conducted by Sol Spiegelman of the University of Illinois, consisted of introducing the viral RNA into a medium containing the RNA's own replication enzyme, plus a supply of raw materials and some salts, and incubating the mixture. When Spiegelman did this, the system obligingly replicated the strands of naked RNA. Spiegelman then extracted some of the freshly synthesized RNA, put it in a separate nutrient solution, and let it multiply. He then decanted some of that RNA into yet another solution, and so on, in a series of steps.
The effect of allowing unrestricted replication was that the RNA that multiplied fastest won out, and got passed on to the "next generation" in the series. The decanting operation therefore replaced, in a highly accelerated way, the basic competition process of Darwinian evolution, acting directly on the RNA. In this respect it resembled an RNA world.
Spiegelman's results were spectacular. As anticipated, copying errors occurred during replication. Relieved of the responsibility of working for a living and the need to manufacture protein coats, the spoon-fed RNA strands began to slim down, shedding parts of the genome that were no longer required and merely proved to be an encumbrance. The RNA molecules that could replicate the fastest simply out-multiplied the competition. After seventy-four generations, what started out as an RNA strand with 4,500 nucleotide bases ended up as a dwarf genome with only 220 bases. This raw replicator with no frills attached could replicate very fast. It was dubbed Spiegelman's monster.
*Evolution at work in the laboratory.
In 1974, Manfred Eigen and his colleagues also experimented with a chemical broth containing Qb replication enzyme and salts, and an energized form of the four bases that make up the building blocks of RNA. They tried varying the quantity of viral RNA initially added to the mixture. As the amount of input RNA was progressively reduced, the experimenters found that, with little competition, it enjoyed untrammeled exponential growth. Even a single RNA molecule added to the broth was enough to trigger a population explosion.
But then something truly amazing was discovered. Replicating strands of RNA were still produced even when not a single molecule of viral RNA was added! To return to my architectural analogy, it was rather like throwing a pile of bricks into a giant mixer and producing, if not a house, then at least a garage. At first Eigen found the results hard to believe, and checked to see whether accidental contamination had occurred. Soon the experimenters convinced themselves that they were witnessing for the first time the spontaneous synthesis of RNA strands form their basic building blocks. Analysis revealed that under some experimental conditions the created RNA resembled Spiegelman's monster.
*Biogenesis in the lab? Well....lets be honest, its not quite biogenesis...its more pre-biogenesis. The RNA would have to form protein skins and develop into cellular organisms.....but its certainly a hint toward biogenesis.
Wednesday, June 13, 2007
More on Evolution....
The Canard: Random Mutation cannot produce complex 'finished' systems.
The Response: Mutations in evolution are not so much 'random' as indifferent, or undirected. There is no predictability or purpose to the mutation that, through natural selection, results in evolution...it just happens.
Jerry Coyne's explanation:
On the basis of much evidence, scientists have concluded that mutations occur randomly. The term "random" here has a specific meaning that is often misunderstood, even by biologists. What we mean is that mutations occur irrespective of whether they would be useful to the organism. Mutations are simply errors in DNA replication. Most of them are harmful or neutral, but a few of them can turn out to be useful. And there is no known biological mechanism for jacking up the probability that a mutation will meet the current adaptive needs of the organism. Bears adapting to snowy terrain will not enjoy a higher probability of getting mutations producing lighter coats than will bears inhabiting non-snowy terrain.
What we do not mean by "random" is that all genes are equally likely to mutate (some are more mutable than others) or that all mutations are equally likely (some types of DNA change are more common than others). It is more accurate, then, to call mutations "indifferent" rather than "random": the chance of a mutation happening is indifferent to whether it would be helpful or harmful. Evolution by selection, then, is a combination of two steps: a "random" (or indifferent) step--mutation--that generates a panoply of genetic variants, both good and bad (in our example, a variety of new coat colors); and then a deterministic step--natural selection--that orders this variation, keeping the good and winnowing the bad (the retention of light-color genes at the expense of dark-color ones).
So....if my imperfect understanding of the explanation is accurate, the following happens:
- Populations reproduce.
- Genetic mutation causes changes in offspring during embryonic formation.
- Offspring who 'chance' to have beneficial mutations that favour their survivability may survive to reproduce more than those with neutral or non-beneficial mutations.
- The population of 'beneficially mutated breeding subjects' is more likely to pass on a beneficial mutation to their offspring (along with other mutations).
- Over time the net accumulation of passed on beneficial traits may lead to a beneficial mutation being adapted by a species and becoming a 'common inheritance' of said species.
- Natural Selection combined with Beneficial Mutations may not result in increased complexity, but in fact may result in the reduction of certain complexities if those reductions amount to a net-positive or net-benefit for the species.
Note: I'm becoming quite a fan of Jerry Coyne.
The Response: Mutations in evolution are not so much 'random' as indifferent, or undirected. There is no predictability or purpose to the mutation that, through natural selection, results in evolution...it just happens.
Jerry Coyne's explanation:
On the basis of much evidence, scientists have concluded that mutations occur randomly. The term "random" here has a specific meaning that is often misunderstood, even by biologists. What we mean is that mutations occur irrespective of whether they would be useful to the organism. Mutations are simply errors in DNA replication. Most of them are harmful or neutral, but a few of them can turn out to be useful. And there is no known biological mechanism for jacking up the probability that a mutation will meet the current adaptive needs of the organism. Bears adapting to snowy terrain will not enjoy a higher probability of getting mutations producing lighter coats than will bears inhabiting non-snowy terrain.
What we do not mean by "random" is that all genes are equally likely to mutate (some are more mutable than others) or that all mutations are equally likely (some types of DNA change are more common than others). It is more accurate, then, to call mutations "indifferent" rather than "random": the chance of a mutation happening is indifferent to whether it would be helpful or harmful. Evolution by selection, then, is a combination of two steps: a "random" (or indifferent) step--mutation--that generates a panoply of genetic variants, both good and bad (in our example, a variety of new coat colors); and then a deterministic step--natural selection--that orders this variation, keeping the good and winnowing the bad (the retention of light-color genes at the expense of dark-color ones).
So....if my imperfect understanding of the explanation is accurate, the following happens:
- Populations reproduce.
- Genetic mutation causes changes in offspring during embryonic formation.
- Offspring who 'chance' to have beneficial mutations that favour their survivability may survive to reproduce more than those with neutral or non-beneficial mutations.
- The population of 'beneficially mutated breeding subjects' is more likely to pass on a beneficial mutation to their offspring (along with other mutations).
- Over time the net accumulation of passed on beneficial traits may lead to a beneficial mutation being adapted by a species and becoming a 'common inheritance' of said species.
- Natural Selection combined with Beneficial Mutations may not result in increased complexity, but in fact may result in the reduction of certain complexities if those reductions amount to a net-positive or net-benefit for the species.
Note: I'm becoming quite a fan of Jerry Coyne.
Wednesday, March 28, 2007
Wednesday, March 21, 2007
Is there a Homosexuality Gene?
Shamelessly Quoted from: http://www.physorg.com/news84720662.html
Is there a homosexuality gene? Discussion at PhysOrgForum
Although biologists are still far from answering this question, scattered evidence for a possible gene influencing sexual orientation has recently encouraged scientists to map out a guide to future research. Because many possibilities for such a gene exist, scientists Sergey Gavrilets and William Rice have recently developed some theoretical guidelines and testable predictions for explaining the evolutionary causes of homosexuality.
“During the 1990s there was a short surge of interest by a small number of labs in finding major genes that might mediate homosexuality,” Rice told PhysOrg.com. “However, for a variety of reasons, this effort waned by the turn of the century. I think that—when studying humans—many people shy away from studying sexual phenotypes in general and homosexuality in particular. Much of Sergey's and my motivation in writing our paper was to rekindle an interest in studying the genetic basis of homosexuality. I personally think that if a firm genetic foundation for homosexuality in humans were established, then many people would view this fascinating human phenotype more objectively.”
During the past several decades, scientists have discovered some interesting patterns that may point toward genetic causes of homosexuality. Among the findings is that male homosexuality appears to be inherited more often from the mother than the father (Pillard). Also, natural selection might maintain a gene that may decrease the fecundity of one sex because the same gene also increases the fecundity of the other sex. In fact, recent data shows that female maternal relatives of gay men have higher than average reproduction capacity (Camperio-Ciani).
Another interesting result from previous research is that a male’s chance of homosexuality increases with the number of biological older brothers he has—even when he grows up away from his older male siblings (Blanchard and Bogaert). Scientists explain that, with each male fetus, a mother develops an increased immunization to an antigen produced by the male fetuses, and this antigen likely plays a role in masculinizing the brain.
These studies and others—while unable to point to a specific gene—do point to the idea that homosexuality may be inherited through a polymorphic gene, which is a gene that has more than one different form, and can exhibit either form. Studies have shown that this gene inheritance must be more complex than for common Mendelian traits.
To take the next step, Gavrilets and Rice have developed several mathematical models that make contrasting predictions for the possible factors responsible for the polymorphism of genes influencing homosexuality. Hopefully, the predictions generated by these models will guide future tests and help zone in on the correct genetic characteristics involved in sexual orientation. As Rice explains, past research has shown the complexity inherent in determining the cause(s) of homosexuality.
“We know that homosexuality (gay or lesbian) can be caused by simple genetic changes in fruit flies, and since so many reproductive and neurological genes are shared by flies and humans, it seems highly likely that there are major genes influencing homosexuality in humans,” said Rice. “However, we also have firm evidence for a birth-order effect on male homosexuality, and discordance in the expression of homosexuality of identical twins, so clearly there is also an environmental influence on the trait.”
Gavrilets and Rice identify two main factors that may explain the polymorphism of a gene (and how the gene spreads): overdominance and sexual antagonism. Overdominance refers to phenotypes that come from heterozygous genes, and the advantages promoting genetic variation. Sexual antagonistic traits are those that are advantageous in one sex, but may cause homosexuality in the other sex. For a variety of different gene inheritance patterns, the scientists provide mathematical models that require, in essence, that the benefits for one sex must outweigh the costs for the other sex.
In their study, Gavrilets and Rice make predictions for the likelihood of certain types of genes (e.g. autosomal or sex-linked, recessive or dominant, with small or large effects) favoring either overdominance or sexual antagonism under different conditions. However, many possibilities remain, and research into each one will determine how well they satisfy the requirements provided in this study.
“The research so far that I think is most illuminating on this topic are the studies showing that homosexuality can have a simple genetic foundation in fruit flies,” said Rice. “I think that it is too early to decide which of our models (or one yet to be formulated) is most feasible. However, based on the abundance of sexually antagonistic variation found in fruit flies, the sexually antagonistic variation seems like a probable candidate process leading to polymorphism for homosexuality.”
Citation: Gavrilets, Sergey and Rice, William R. “Genetic models of homosexuality: generating testable predictions.” Proceedings of the Royal Society B (2006) 273, 3031-3038.
By Lisa Zyga, Copyrght 2006 PhysOrg.com
Is there a homosexuality gene? Discussion at PhysOrgForum
Although biologists are still far from answering this question, scattered evidence for a possible gene influencing sexual orientation has recently encouraged scientists to map out a guide to future research. Because many possibilities for such a gene exist, scientists Sergey Gavrilets and William Rice have recently developed some theoretical guidelines and testable predictions for explaining the evolutionary causes of homosexuality.
“During the 1990s there was a short surge of interest by a small number of labs in finding major genes that might mediate homosexuality,” Rice told PhysOrg.com. “However, for a variety of reasons, this effort waned by the turn of the century. I think that—when studying humans—many people shy away from studying sexual phenotypes in general and homosexuality in particular. Much of Sergey's and my motivation in writing our paper was to rekindle an interest in studying the genetic basis of homosexuality. I personally think that if a firm genetic foundation for homosexuality in humans were established, then many people would view this fascinating human phenotype more objectively.”
During the past several decades, scientists have discovered some interesting patterns that may point toward genetic causes of homosexuality. Among the findings is that male homosexuality appears to be inherited more often from the mother than the father (Pillard). Also, natural selection might maintain a gene that may decrease the fecundity of one sex because the same gene also increases the fecundity of the other sex. In fact, recent data shows that female maternal relatives of gay men have higher than average reproduction capacity (Camperio-Ciani).
Another interesting result from previous research is that a male’s chance of homosexuality increases with the number of biological older brothers he has—even when he grows up away from his older male siblings (Blanchard and Bogaert). Scientists explain that, with each male fetus, a mother develops an increased immunization to an antigen produced by the male fetuses, and this antigen likely plays a role in masculinizing the brain.
These studies and others—while unable to point to a specific gene—do point to the idea that homosexuality may be inherited through a polymorphic gene, which is a gene that has more than one different form, and can exhibit either form. Studies have shown that this gene inheritance must be more complex than for common Mendelian traits.
To take the next step, Gavrilets and Rice have developed several mathematical models that make contrasting predictions for the possible factors responsible for the polymorphism of genes influencing homosexuality. Hopefully, the predictions generated by these models will guide future tests and help zone in on the correct genetic characteristics involved in sexual orientation. As Rice explains, past research has shown the complexity inherent in determining the cause(s) of homosexuality.
“We know that homosexuality (gay or lesbian) can be caused by simple genetic changes in fruit flies, and since so many reproductive and neurological genes are shared by flies and humans, it seems highly likely that there are major genes influencing homosexuality in humans,” said Rice. “However, we also have firm evidence for a birth-order effect on male homosexuality, and discordance in the expression of homosexuality of identical twins, so clearly there is also an environmental influence on the trait.”
Gavrilets and Rice identify two main factors that may explain the polymorphism of a gene (and how the gene spreads): overdominance and sexual antagonism. Overdominance refers to phenotypes that come from heterozygous genes, and the advantages promoting genetic variation. Sexual antagonistic traits are those that are advantageous in one sex, but may cause homosexuality in the other sex. For a variety of different gene inheritance patterns, the scientists provide mathematical models that require, in essence, that the benefits for one sex must outweigh the costs for the other sex.
In their study, Gavrilets and Rice make predictions for the likelihood of certain types of genes (e.g. autosomal or sex-linked, recessive or dominant, with small or large effects) favoring either overdominance or sexual antagonism under different conditions. However, many possibilities remain, and research into each one will determine how well they satisfy the requirements provided in this study.
“The research so far that I think is most illuminating on this topic are the studies showing that homosexuality can have a simple genetic foundation in fruit flies,” said Rice. “I think that it is too early to decide which of our models (or one yet to be formulated) is most feasible. However, based on the abundance of sexually antagonistic variation found in fruit flies, the sexually antagonistic variation seems like a probable candidate process leading to polymorphism for homosexuality.”
Citation: Gavrilets, Sergey and Rice, William R. “Genetic models of homosexuality: generating testable predictions.” Proceedings of the Royal Society B (2006) 273, 3031-3038.
By Lisa Zyga, Copyrght 2006 PhysOrg.com
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