Finding: The Peppered Moth has been used as an example of evolution in action. Recent controversy about the precise mechanism used to change the appearance of the Peppered Moth has allowed creationists to argue that Evolutionists have used an incorrect and fraudulent example of evolution. but new research has confirmed the actual environmental process used by evolution to change the appearance of the Peppered Moth.
An Example of Evolution in Action
For decades, the peppered moth was the textbook example of evolution in action, unassailable proof that Darwin got it right.
Recently, though, the peppered moth's status as an icon of evolution has been under threat. Emboldened by legitimate scientific debate over the fine details of the peppered moth story, creationists and other anti-evolutionists have orchestrated a decade-long campaign to discredit it - and with it the entire edifice of evolution.
These days you're less likely to hear about the peppered moth as proof of evolution than as proof that biologists cannot get their story straight.
Recent Controversy
The peppered moth now counts among the anti-evolutionists' most potent weapons. In the past few years it has helped them get material critical of evolution added to high-school science lessons in Ohio and Kansas, although the material has now been removed. In 2000, the authors of the widely used school textbook Biology reluctantly dropped the peppered moth in direct response to creationist attacks. The latest edition features the beaks of Galapagos finches instead.
Now, though, biologists are fighting back. Majerus recently finished an exhaustive experiment designed to repair the peppered moth's tattered reputation and reverse the creationists' advances. The preliminary results are out, and Majerus says they are enough to fully reinstate the moth as the prime example of Darwinian evolution in action.
The Peppered Moth Evolutionary Story
The textbook version of the peppered moth story is simple enough. Before the mid-19th century, all peppered moths in England were cream coloured with dark spots. In 1848, however, a "melanic" form was caught and pinned by a moth collector in Manchester. By the turn of the 20th century melanic moths had all but replaced the light form in Manchester and other industrial regions of England. The cause of the change was industrial pollution: as soot and other pollutants filled the air, trees used by peppered moths as daytime resting places were stripped of their lichens then stained black with soot. Light-coloured moths that were well camouflaged on lichen-coated trees were highly conspicuous on blackened trees. Melanic moths, in contrast, were less easily spotted by predatory birds and so survived longer, leaving more offspring than the light forms. As melanism is heritable, over time the proportion of black moths increased.
As with all textbook examples, however, this is a simplified account of decades of field work, genetic studies and mathematical analyses carried out by dozens of researchers. It also draws disproportionately on the flawed work of one biologist, Bernard Kettlewell of the University of Oxford.
1950 Experiments
In the 1950s Kettlewell carried out a series of classic experiments that cemented the peppered moth's iconic status. These were designed to test a hypothesis first proposed that the rise in melanism was a result of natural selection caused by differential bird predation.
Kettlewell carried out experiments in 1953 and 1955 in polluted woodland in Rubery, near Birmingham, and unspoiled woodland in rural Dorset. In the mornings he dropped hundreds of marked moths, both light and melanic, on tree trunks, where they quickly took up resting positions. In the evenings he used moth traps to recapture them. In Birmingham, he recaptured twice as many dark as light moths. In Dorset, he found the opposite, recapturing more light moths. The obvious conclusion was that light moths were more heavily predated than dark moths in Birmingham, and vice versa in Dorset.
During these experiments Kettlewell also directly observed robins and hedge sparrows eating peppered moths. As expected, the birds noticed and ate more light-coloured moths on soot-covered trees, and more melanic ones on lichen-covered trees. This was a breakthrough, as hardly anyone in Kettlewell's time believed that birds ate moths.
Kettlewell's experiments were accepted as proof that the rise of the melanic moth was a case of evolution by natural selection, and that the agent of selection was bird predation. The peppered moth quickly found its way into textbooks, often accompanied by striking photographs of light and dark moths resting on lichen-covered and soot-stained bark.
Problems with the Experiments
But in truth there were problems with Kettlewell's experiments. Perhaps the most significant was that he released moths onto tree trunks. Although moths occasionally choose trunks as a daytime resting place, they prefer the underside of branches. Kettlewell also let his moths go during the day, even though they normally choose their resting place at night. And he released more moths than would naturally be present in an area, which may have made them more conspicuous and tempted birds to eat them even if they wouldn't normally. These problems were familiar to evolutionary biologists, many of whom tried to resolve them with experiments, but were not given a general airing until 1998, when Majerus pointed out the flaws in Kettlewell's work in his book Melanism: Evolution in action.
The Origins of the Controversy
In November 1998, Nature published a review of his book by evolutionary biologist Jerry Coyne of the University of Chicago. In it, Coyne wrote a sentence that would come back to haunt him: "For the time being we must discard Biston as a well-understood example of natural selection in action." He did not mean to imply that the peppered moth was not an example of evolution by natural selection, merely that the fine details were still lacking. "I wasn't very clear. The key was well-understood."
But to anti-evolution organisations such as the Discovery Institute, they took the criticism of the Kettewell experiments. Coyne's words were taken out of context and were selectively quoting him and Majerus they managed to portray the textbook version of events as hopelessly flawed, and with it the entire theory of evolution. They also pointed at the textbook pictures - which are often staged with dead specimens - and proclaimed that the science behind those pictures was staged too.
Out of the Frying Pan into the Fire
In 2000 Majerus embarked on a large experiment designed to iron out the problems with Kettlewell's work. But things took a turn for the worse when in 2002, journalist Judith Hooper published a popular science book called Of Moths and Men: Intrigue, tragedy & the peppered moth. She accused Kettlewell of manipulating his data to prove his hypothesis. Hooper's book is not a creationist text, but creationists seized on it anyway as evidence that Kettlewell was a fraud.
Promlems with Hooper's Book
Numerous historians and scientists pointed out that Hooper's book is littered with factual errors, not least the accusation that Kettlewell forged his data. There is no evidence he did so. Coyne himself wrote a scathing review of Hooper's book in which he accused her of unfairly smearing Kettlewell and concluded that "industrial melanism still represents a splendid example of evolution in action". It is fair to say that this accurately represented the views of the vast majority of evolutionary biologists at the time, but by then the damage had been done.
Reworking the Experiments
Meanwhile, Majerus was steadily working through his experiment in his own garden in Cambridge. He started by identifying 103 branches that were suitable resting places for peppered moths, ranging in height from 2 to 26 metres, many of them covered in lichen. For seven years, every night from May to August, he placed nets around 12 randomly chosen branches and released a single moth into each net. Around 90 per cent were light-coloured to reflect the natural frequencies of the two forms around Cambridge.
The moths took up resting positions overnight, usually on the underside of the branch. At sunrise the next morning Majerus removed the nets and 4 hours later checked to see which moths were still there. His assumption was that, as peppered moths spend the whole day in their resting position, any that disappeared between sunrise and mid-morning had almost certainly been spotted and eaten by birds.
Because he was able to watch some of the branches from his house through binoculars, he also observed the moths being eaten by many species of bird - including robins, blackbirds, magpies and blue tits. As expected, the birds were better at spotting the dark moths than the camouflaged light ones, he says.
Majerus addressed all the flaws in Kettlewell's experiments. He let moths choose their own resting positions, he used low densities, he released them at night when they were normally active, and he used local moths at the frequencies found in nature.
Majerus presented his preliminary results at a meeting of evolutionary biologists at the University of Uppsala in Sweden. He said that over the seven years, 29 per cent of his melanic moths were eaten compared with 22 per cent of light ones. This was a statistically significant difference.
As in many parts of the UK, pollution in Cambridge has declined since the adoption of clean air acts in the 1950s, and melanic moths are becoming increasingly rare, declining from 12 per cent of the population in 2001 to under 2 per cent today. According to Majerus, his results show that bird predation is the agent of this change. Birds were better at spotting dark moths than light ones, ate more of them and reduced the percentage of black moths over time. It provides the proof of evolution.
There is no doubt that the peppered moth's colour is genetically determined, so changes in the frequencies of light and dark forms demonstrate changes in gene frequencies - and that is evolution. What's more, the direction and speed at which this evolution occurred can only be explained by natural selection.
Anti-evolutionists continue to suggest there is, of course, but as far as Majerus and others are concerned their claims have been debunked and the peppered moth should be reinstated as a textbook example of evolution in action. Not just to teach children either, but also as a direct rebuttal of anti-evolutionism. The peppered moth story is easy to understand because it involves things that we are familiar with: vision and predation and birds and moths and pollution and camouflage and lunch and death. That is why the anti-evolution lobby attacks the peppered moth story. They are frightened that too many people will be able to understand.
Friday, August 22, 2008
Some problems with Intelligent Design
Is this the only way that life could have originated?
Intelligent design advocates make the case that the universe is finely tuned, so much so that if you changed some small feature, the gravitational constant, or the mass of the proton, then the universe would be different, and life could not have been formed. They conclude that the intelligent construction of the universe, so finely tuned, creates proof that the universe was created by an intelligent creator. In other words, the intelligent creation is the result of an intelligent creator. The universe is intelligently designed, so there must be an intelligent creator, or God.
Let's look at this arguement. The main thrust of the argument is that because the universe, with it's natural construction of atoms has resulted in an organized table of periodic elements, and one of them, carbon, is the foundation of life, this natural construction could not have occured if the resulting organization weren't put into place to begin with.
Let's see.
Let's talk about Baseball. In baseball, the home plate is 90 feet from first base. Batters have their entire careers built around getting to first base as soon as possible after they hit the ball.
Good batters will get there about 30% of the time. Bad batters will get there about 20% of the time. Most batters will fall in between those two percentages.
Now let's change the dimensions of the ball field. Now say that the distance is not 90 feet but 89 feet. That means that more players will get to first base. Averages my go up so the the best hitters are over 35% and the worst hitters are now batting over 25%. The statistics have changed and the players will have to adjust their game to the new dimensions.
Or suppose the length is not 90 feet but 91 feet. The opposite will occur. More players will be out. Batting averages will drop, so that the best hitters are now batting around 25%; the worst hitters are batting around 15%. Again the statistics change, and the players have to adjust to the new dimensions.
But in both cases the game of baseball is still recognized. The conditions change but the game is still there. So let's take this kind of argument and apply it to the universe.
We also know that element # 6 is carbon. And carbon is the foundation of life.
Universe #2:
Now let's suppose that in Universe #2, there was a big bang as well. But this time the constant of the universe is 1.1C. It is just a little bit bigger than C is in our universe. One of the consequences is that there are 134 naturally occurring elements. Carbon is one of them, but in this universe, element #48, our "Cadmium" is responsible for life, not carbon. Again in this universe there was a naturally occuring structure built around how the atoms were arranged. Life was not pre-ordained to start with Carbon, but with a different element.
Universe #3.
Universe #3 is like universe #2 and Universe #1. But in universe #3, the constant is .98C, smaller than universe #1. As a result there are only 58 naturally occuring elements, and element #18, "Argon" creates life. And again with this universe, the atoms arranged in such away that the properties of the periodic table result in a very different configuration for what constitutes matter.
In all three universes, we see that it is not necessary to invoke a special design, or even that the design in one is unique. This means that an intelligent design in which there is only one way to create life, doesn't have to be.
Intelligent design advocates make the case that the universe is finely tuned, so much so that if you changed some small feature, the gravitational constant, or the mass of the proton, then the universe would be different, and life could not have been formed. They conclude that the intelligent construction of the universe, so finely tuned, creates proof that the universe was created by an intelligent creator. In other words, the intelligent creation is the result of an intelligent creator. The universe is intelligently designed, so there must be an intelligent creator, or God.
Let's look at this arguement. The main thrust of the argument is that because the universe, with it's natural construction of atoms has resulted in an organized table of periodic elements, and one of them, carbon, is the foundation of life, this natural construction could not have occured if the resulting organization weren't put into place to begin with.
Let's see.
Let's talk about Baseball. In baseball, the home plate is 90 feet from first base. Batters have their entire careers built around getting to first base as soon as possible after they hit the ball.
Good batters will get there about 30% of the time. Bad batters will get there about 20% of the time. Most batters will fall in between those two percentages.
Now let's change the dimensions of the ball field. Now say that the distance is not 90 feet but 89 feet. That means that more players will get to first base. Averages my go up so the the best hitters are over 35% and the worst hitters are now batting over 25%. The statistics have changed and the players will have to adjust their game to the new dimensions.
Or suppose the length is not 90 feet but 91 feet. The opposite will occur. More players will be out. Batting averages will drop, so that the best hitters are now batting around 25%; the worst hitters are batting around 15%. Again the statistics change, and the players have to adjust to the new dimensions.
But in both cases the game of baseball is still recognized. The conditions change but the game is still there. So let's take this kind of argument and apply it to the universe.
Universe #1
About 13 to 15 billion years ago, the big bang occurred. And let's say that one of the results of the big bang was that certain rules, and physical laws and constants were created that made the universe the way that it is. Let's call the rules and conditions by a simple term: "C" which the constant for the speed of light.
We also know that element # 6 is carbon. And carbon is the foundation of life.
Universe #2:
Now let's suppose that in Universe #2, there was a big bang as well. But this time the constant of the universe is 1.1C. It is just a little bit bigger than C is in our universe. One of the consequences is that there are 134 naturally occurring elements. Carbon is one of them, but in this universe, element #48, our "Cadmium" is responsible for life, not carbon. Again in this universe there was a naturally occuring structure built around how the atoms were arranged. Life was not pre-ordained to start with Carbon, but with a different element.
Universe #3.
Universe #3 is like universe #2 and Universe #1. But in universe #3, the constant is .98C, smaller than universe #1. As a result there are only 58 naturally occuring elements, and element #18, "Argon" creates life. And again with this universe, the atoms arranged in such away that the properties of the periodic table result in a very different configuration for what constitutes matter.
In all three universes, we see that it is not necessary to invoke a special design, or even that the design in one is unique. This means that an intelligent design in which there is only one way to create life, doesn't have to be.
Tuesday, July 22, 2008
New Method Of Selecting DNA Microarray-based Genomic Selection (MGS),
Finding: Microarray-based Genomic Selection (MGS), is a research protocol that allows scientists to extract and enrich specific large-sized DNA regions, then compare genetic variation among individuals using DNA resequencing methods. Sequencing can be done by a small staff of researchers...it is inexpensive and not labor intensive.
The new technology will allow researchers to more easily discover subtle and overlooked genetic variations that may have serious consequences for health and disease.
Problem in genetic investigation
DNA sequencing platforms do not have a simple, inexpensive method of selecting specific regions to resequence; this has been a serious barrier to detecting subtle genetic variability among individuals.
The goal of most human genetics researchers is to find variations in the genome that contribute to disease. Despite the success of the human genome project and the availability of a number of next-generation The Emory scientists believe that goal will be much more obtainable thanks to MGS.
MGS uses DNA oligonucleotides (probes) arrayed on a chip at high density (microarray) to directly capture and extract the target region(s) from the genome. The probes are chosen from the reference human genome and are complementary to the target(s) to capture. Once the target is selected, resequencing arrays or other sequencing technologies can be used to identify variations.
The Emory scientists believe MGS will allow them to easily compare genetic variation among a number of individuals and relate that variation to health and disease.
The human genome project focused on sequencing just one human genome--an amazing technological feat that required a very large industrial infrastructure, hundreds of people and a great deal of money. The question since then has been, can we replicate the ability to resequence parts of the genome, or ultimately the entire genome, in a laboratory with a single investigator and a small staff" The answer is now 'yes.'"
Geneticists have found many different types of obvious gene mutations that are deleterious to health, but more subtle variations, or variations located in parts of the genome where scientists rarely look, may also have negative consequences but are not so easily discovered.
Other methods for isolating and studying a particular region of the genome, such as PCR and BAC cloning (bacterial artificial chromosomes) are comparatively labor intensive, difficult for single laboratories to scale to large sections of the genome, and relatively expensive, says Dr. Zwick.
Whereas typical microarray technology measures gene expression, MGS is a novel use of microarrays for capturing specific genomic sequences. For the published study, a third type of microarray--a resequencing array--was used to determine the DNA sequence in the patient samples.
The logic behind the resequencing chip is that you design the chip to have the identity of the base at every single site in a reference sequence. You use the human genome reference sequence as a shell and you search for variation on the theme. This alternative new technology allows a regular-sized laboratory and single investigator to generate a great deal of data at a cost significantly less than what a sequencing center would charge.
The new technology will allow researchers to more easily discover subtle and overlooked genetic variations that may have serious consequences for health and disease.
Problem in genetic investigation
DNA sequencing platforms do not have a simple, inexpensive method of selecting specific regions to resequence; this has been a serious barrier to detecting subtle genetic variability among individuals.
The goal of most human genetics researchers is to find variations in the genome that contribute to disease. Despite the success of the human genome project and the availability of a number of next-generation The Emory scientists believe that goal will be much more obtainable thanks to MGS.
MGS uses DNA oligonucleotides (probes) arrayed on a chip at high density (microarray) to directly capture and extract the target region(s) from the genome. The probes are chosen from the reference human genome and are complementary to the target(s) to capture. Once the target is selected, resequencing arrays or other sequencing technologies can be used to identify variations.
The Emory scientists believe MGS will allow them to easily compare genetic variation among a number of individuals and relate that variation to health and disease.
The human genome project focused on sequencing just one human genome--an amazing technological feat that required a very large industrial infrastructure, hundreds of people and a great deal of money. The question since then has been, can we replicate the ability to resequence parts of the genome, or ultimately the entire genome, in a laboratory with a single investigator and a small staff" The answer is now 'yes.'"
Geneticists have found many different types of obvious gene mutations that are deleterious to health, but more subtle variations, or variations located in parts of the genome where scientists rarely look, may also have negative consequences but are not so easily discovered.
Other methods for isolating and studying a particular region of the genome, such as PCR and BAC cloning (bacterial artificial chromosomes) are comparatively labor intensive, difficult for single laboratories to scale to large sections of the genome, and relatively expensive, says Dr. Zwick.
Whereas typical microarray technology measures gene expression, MGS is a novel use of microarrays for capturing specific genomic sequences. For the published study, a third type of microarray--a resequencing array--was used to determine the DNA sequence in the patient samples.
The logic behind the resequencing chip is that you design the chip to have the identity of the base at every single site in a reference sequence. You use the human genome reference sequence as a shell and you search for variation on the theme. This alternative new technology allows a regular-sized laboratory and single investigator to generate a great deal of data at a cost significantly less than what a sequencing center would charge.
Friday, June 20, 2008
Importance Of Gene Regulation For Common Human Disease
Finding: A new study shows that common, complex diseases are more likely to be due to genetic variation in regions that control activity of genes, rather than in the regions that specify the protein code.
Where are the regions?
This result comes from a study of the activity of almost 14,000 genes in 270 DNA samples collected for the HapMap Project. The authors looked at 2.2 million DNA sequence variants (SNPs) to determine which affected gene activity. They found that activity of more than 1300 genes was affected by DNA sequence changes in regions predicted to be involved in regulating gene activity, which often lie close to, but outside, the protein-coding regions.
The challenge of large-scale studies that link a DNA variant to a disease
We predict that variants in regulatory regions make a greater contribution to complex disease than do variants that affect protein sequence. This is the first study on this scale and these results are confirming our intuition about the nature of natural variation in complex traits.
One of the challenges of large-scale studies that link a DNA variant to a disease is to determine how the variant causes the disease: our analysis will help to develop that understanding, a vital step on the path from genetics to improvements in healthcare.
What the HapMap does
Past studies of rare, monogenic disease, such as cystic fibrosis and sickle-cell anaemia, have focused on changes to the protein-coding regions of genes because they have been visible to the tools of human genetics. With the HapMap and large-scale research methods, researchers can inspect the role of regions that regulate activity of many thousands of genes.
The HapMap Project established cell cultures from participants from four populations as well as, for some samples, information from families, which can help to understand inheritance of genetic variation. The team used these resources to study gene activity in the cell cultures and tie that to DNA sequence variation
Scientists found strong evidence that SNP variation close to genes - where most regulatory regions lie - could have a dramatic effect on gene activity. Although many effects were shared among all four HapMap populations, they also shown that a significant number were restricted to one population.
What about the house keeping genes?
They also showed that genes required for the basic functions of the cell - so-called housekeeping genes - were less likely to be subject to genetic variation. This was exactly as one would expect: you can't mess too much with the fundamental life processes and we predicted we would find reduced effects on these genes.
The study also detected SNP variants that affect the activity of genes located a great distance away. Genetic regulation in the human genome is complex and highly variable: a tool to detect such distant effects will expand the search for causative variants. The authors note, however, that the small sample size of 270 HapMap individuals is sensitive enough to detect only the strongest effects.
Where are the regions?
This result comes from a study of the activity of almost 14,000 genes in 270 DNA samples collected for the HapMap Project. The authors looked at 2.2 million DNA sequence variants (SNPs) to determine which affected gene activity. They found that activity of more than 1300 genes was affected by DNA sequence changes in regions predicted to be involved in regulating gene activity, which often lie close to, but outside, the protein-coding regions.
The challenge of large-scale studies that link a DNA variant to a disease
We predict that variants in regulatory regions make a greater contribution to complex disease than do variants that affect protein sequence. This is the first study on this scale and these results are confirming our intuition about the nature of natural variation in complex traits.
One of the challenges of large-scale studies that link a DNA variant to a disease is to determine how the variant causes the disease: our analysis will help to develop that understanding, a vital step on the path from genetics to improvements in healthcare.
What the HapMap does
Past studies of rare, monogenic disease, such as cystic fibrosis and sickle-cell anaemia, have focused on changes to the protein-coding regions of genes because they have been visible to the tools of human genetics. With the HapMap and large-scale research methods, researchers can inspect the role of regions that regulate activity of many thousands of genes.
The HapMap Project established cell cultures from participants from four populations as well as, for some samples, information from families, which can help to understand inheritance of genetic variation. The team used these resources to study gene activity in the cell cultures and tie that to DNA sequence variation
Scientists found strong evidence that SNP variation close to genes - where most regulatory regions lie - could have a dramatic effect on gene activity. Although many effects were shared among all four HapMap populations, they also shown that a significant number were restricted to one population.
What about the house keeping genes?
They also showed that genes required for the basic functions of the cell - so-called housekeeping genes - were less likely to be subject to genetic variation. This was exactly as one would expect: you can't mess too much with the fundamental life processes and we predicted we would find reduced effects on these genes.
The study also detected SNP variants that affect the activity of genes located a great distance away. Genetic regulation in the human genome is complex and highly variable: a tool to detect such distant effects will expand the search for causative variants. The authors note, however, that the small sample size of 270 HapMap individuals is sensitive enough to detect only the strongest effects.
Tuesday, June 17, 2008
Happenstance mutations matter
Scientists show that happenstance mutations matter
Finding: In experiments on bacteria grown in the lab, scientists found that evolving a new trait sometimes depended on previous, happenstance mutations. Without those earlier random mutations, the window of opportunity for the novel trait would never have opened. History might have been different.
Evolutionist Stephen Jay Gould once suggested that the if the evolution of life were “wound back” and played again from the start, it could have turned out very differently.
Though not firmly conclusive, the new research adds a real-world case study of evolution in action to the decades-old debate stirred by Gould’s thought experiment. British paleontologist Simon Conway Morris and others argued that only a few optimal solutions exist for an organism to adapt to its environment, so even if the clock were wound back, environmental pressures would eventually steer evolution toward one of those solutions — regardless of the randomness along the way.
What the scientists did
Scientists obviously can’t turn back the hands of time, but Richard Lenski and his colleagues at Michigan State University in East Lansing did the next best thing. Lenski’s team watched 12 colonies of identical E. coli bacteria evolve under carefully controlled lab conditions for 20 years, which equates to more than 40,000 generations of bacteria. After every 500 generations, the researchers froze samples of bacteria. Those bacteria could later be thawed out to “replay” the evolutionary clock from that point in time.
The evolution of a nutrient absorption ability
After about 31,500 generations, one colony of bacteria evolved the novel ability to use a nutrient that E. coli normally can’t absorb from its environment. Thawed-out samples from after the 20,000-generation mark were much more likely to re-evolve this trait than earlier samples, which suggests that an unnoticed mutation that occurred around the 20,000th generation enabled the microbes to later evolve the nutrient-absorption ability through a second mutation, the researchers report in the Proceedings of the National Academy of Sciences.
By way of contrast with another control group
In the 11 other colonies, this earlier mutation didn’t occur, so the evolution of this novel ability never happened.
Put populations in the same environment and see what happens
This is a direct empirical demonstration of Gould-like contingency in evolution. You can’t do an exact replay in nature, but scientists were able to literally put all these populations in virtually identical environments and show that contingency is really what had occurred.
What was the mutation that occured?
The next step will be to determine what that earlier mutation was and how it made the later change possible. If the first mutation didn’t offer any survival advantage to the microbes on its own, it would make the case airtight that Gould was right. That’s because a mutation that doesn’t improve an organism’s ability to survive and reproduce can’t be favored by evolution, so whether the microbe happens to have that necessary mutation when the second evolutionary change occurs becomes purely a matter of chance. Thus the first mutation must have improved the chance of the organisms survival.
The first mutation gave the microbes a survival advantage. The growth rate and the density of bacteria in the colony jumped up after the second mutation, but not after the first one. The first mutation may have set the stage for what was to come, the second mutation took advantage of the change.
Finding: In experiments on bacteria grown in the lab, scientists found that evolving a new trait sometimes depended on previous, happenstance mutations. Without those earlier random mutations, the window of opportunity for the novel trait would never have opened. History might have been different.
Evolutionist Stephen Jay Gould once suggested that the if the evolution of life were “wound back” and played again from the start, it could have turned out very differently.
Though not firmly conclusive, the new research adds a real-world case study of evolution in action to the decades-old debate stirred by Gould’s thought experiment. British paleontologist Simon Conway Morris and others argued that only a few optimal solutions exist for an organism to adapt to its environment, so even if the clock were wound back, environmental pressures would eventually steer evolution toward one of those solutions — regardless of the randomness along the way.
What the scientists did
Scientists obviously can’t turn back the hands of time, but Richard Lenski and his colleagues at Michigan State University in East Lansing did the next best thing. Lenski’s team watched 12 colonies of identical E. coli bacteria evolve under carefully controlled lab conditions for 20 years, which equates to more than 40,000 generations of bacteria. After every 500 generations, the researchers froze samples of bacteria. Those bacteria could later be thawed out to “replay” the evolutionary clock from that point in time.
The evolution of a nutrient absorption ability
After about 31,500 generations, one colony of bacteria evolved the novel ability to use a nutrient that E. coli normally can’t absorb from its environment. Thawed-out samples from after the 20,000-generation mark were much more likely to re-evolve this trait than earlier samples, which suggests that an unnoticed mutation that occurred around the 20,000th generation enabled the microbes to later evolve the nutrient-absorption ability through a second mutation, the researchers report in the Proceedings of the National Academy of Sciences.
By way of contrast with another control group
In the 11 other colonies, this earlier mutation didn’t occur, so the evolution of this novel ability never happened.
Put populations in the same environment and see what happens
This is a direct empirical demonstration of Gould-like contingency in evolution. You can’t do an exact replay in nature, but scientists were able to literally put all these populations in virtually identical environments and show that contingency is really what had occurred.
What was the mutation that occured?
The next step will be to determine what that earlier mutation was and how it made the later change possible. If the first mutation didn’t offer any survival advantage to the microbes on its own, it would make the case airtight that Gould was right. That’s because a mutation that doesn’t improve an organism’s ability to survive and reproduce can’t be favored by evolution, so whether the microbe happens to have that necessary mutation when the second evolutionary change occurs becomes purely a matter of chance. Thus the first mutation must have improved the chance of the organisms survival.
The first mutation gave the microbes a survival advantage. The growth rate and the density of bacteria in the colony jumped up after the second mutation, but not after the first one. The first mutation may have set the stage for what was to come, the second mutation took advantage of the change.
Monday, May 26, 2008
BAC: Super-Sized Inserts
Bacterial Artificial Chromosomes (BAC) have been developed to hold much larger pieces of DNA than a plasmid can. BAC vectors were originally created from part of an unusual plasmid present in some bacteria called the F’ plasmid.
The F’ plasmid allows bacteria to have “sex” (well, sort of: F’ helps bacteria give its genome to another bacteria but this only happens rarely when bacteria are under a lot of stress). F’ had been studied extensively and it was found that it could hold up to a million basepairs of DNA from another bacteria. Also, F’ has origins of replication and bacteria have a way to control how F’ is copied.
The F’ plasmid allows bacteria to have “sex” (well, sort of: F’ helps bacteria give its genome to another bacteria but this only happens rarely when bacteria are under a lot of stress). F’ had been studied extensively and it was found that it could hold up to a million basepairs of DNA from another bacteria. Also, F’ has origins of replication and bacteria have a way to control how F’ is copied.
Friday, May 16, 2008
Mitochondrial Eve
'Mitochondrial Eve' Research: Humanity Was Genetically Divided For 100,000 Years
A Picture of the Ancient Past
Finding:
Based on Anthroopological genetic research, researchers believe that about 60,000 years ago, modern humans started the journey to populate the world. However, relatively little is known about the demographic history of our species over the previous 140,000 years in Africa.
The current study focuses on Africa and refines the understanding of early modern Homo sapiens history. These early human populations were small and isolated from each other for many tens of thousands of years.
The research was based on a survey of African mitochondrial DNA (mtDNA) and is the most extensive survey of its kind. It included over 600 complete mtDNA genomes from indigenous populations across the continent.
How Old Was “Mitochondrial Eve”?
MtDNA, inherited down the maternal line, was used in 1987 to discover the age of the “Mitochondrial Eve,” the most recent common female ancestor of everyone alive today. This work has since been extended to show unequivocally that “Mitochondrial Eve” was an African woman who lived sometime during the past 200,000 years.
Recent data suggests that Eastern Africa went through a series of massive droughts between 90,000 and 135,000 years ago. It is possible that this climate shift contributed to the population splits. What is surprising is the length of time the populations were separate — for as much as half of our entire history as a species.
The study shows that tiny bands of early humans, forced apart by harsh environmental conditions, coming back from the brink to reunite and populate the world. Truly an epic drama, written in our DNA.
A Picture of the Ancient Past
Finding:
Based on Anthroopological genetic research, researchers believe that about 60,000 years ago, modern humans started the journey to populate the world. However, relatively little is known about the demographic history of our species over the previous 140,000 years in Africa.
The current study focuses on Africa and refines the understanding of early modern Homo sapiens history. These early human populations were small and isolated from each other for many tens of thousands of years.
The research was based on a survey of African mitochondrial DNA (mtDNA) and is the most extensive survey of its kind. It included over 600 complete mtDNA genomes from indigenous populations across the continent.
How Old Was “Mitochondrial Eve”?
MtDNA, inherited down the maternal line, was used in 1987 to discover the age of the “Mitochondrial Eve,” the most recent common female ancestor of everyone alive today. This work has since been extended to show unequivocally that “Mitochondrial Eve” was an African woman who lived sometime during the past 200,000 years.
Recent data suggests that Eastern Africa went through a series of massive droughts between 90,000 and 135,000 years ago. It is possible that this climate shift contributed to the population splits. What is surprising is the length of time the populations were separate — for as much as half of our entire history as a species.
The study shows that tiny bands of early humans, forced apart by harsh environmental conditions, coming back from the brink to reunite and populate the world. Truly an epic drama, written in our DNA.
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