It is understood that in the field of molecular evolution new genes can only evolve from duplicated or rearranged versions of preexisting genes. Furthermore, it seemed unlikely that evolutionary processes could produce a functional protein-coding gene from what was once inactive DNA.
But that view is changing as some evidence suggests that this phenomenon does in fact occur. It has been found that genes have arisen from non-coding DNA in yeast,flies, and also primates. No such genes had been found to be unique to humans until now, and the discovery raises questions about how these genes might make humans different from other primates.
One gene was identified in chronic lymphocytic leukemia. This is the first evidence for entirely novel human-specific protein-coding genes originating from ancestrally noncoding sequences. A non-coding sequence involves RNA (ncRNA) is a molecule that is not translated into a protein.In other words, a gene that was once dormant is now active.
The consequence of the finding is that while many coding sequences exist, there are some that are dormant in primates, but become active in humans. This makes us different
Showing posts with label Genes. Show all posts
Showing posts with label Genes. Show all posts
Friday, September 11, 2009
Wednesday, January 23, 2008
Thursday, December 20, 2007
Evolution With A Restricted Number Of Genes
Finding: RNA polymerase II is highly conserved through evolution, with many of its structural characteristics being conserved between bacteria and humans. The development of higher forms of life would appear to have been influenced by RNA polymerase II. This enzyme transcribes the information coded by genes from DNA into messenger-RNA (mRNA), which in turn is the basis for the production of proteins.
Single-Cell Organisms and the Problem of Complexity
Single-cell organisms were already in existence 500 million years ago, with several thousand genes providing different cellular functions. Further developments seemed dependent on producing even more genes.
It would appear that for a highly developed organism like a human, this form of evolution would have resulted in several million genes. But researchers were surprised to learn, following publication of the human genome, that a human only has around 25,000 genes – not many more than a fruit fly or a worm with approximately 15,000 to 20,000 genes.
It would appear that, over the last 500 million years, other ways to produce highly complex organisms have evolved. Evolution has simply found more efficient ways to use the genes already there. But what could have made this possible?
Is there an answer? Yes - it involves the RNA
New results represent a piece of the puzzle and shed new light on to the purpose of an unusual structure in RNA polymerase II.
They build on earlier observations that gene expression is not just regulated by binding of the enzyme to the gene locus to which it is recruited, but also during the phase of active transcription from DNA into RNA. During this phase, parts of the newly synthesised RNA may be removed and the remaining sequences combined into new RNA message. This ‘splicing’ of RNA occurs during gene transcription, and in extreme cases, can produce RNAs coding for several thousand different proteins from a single gene.
How it Works - The Development of CTD
But what was the development that permitted this advance in gene usage? The RNA polymerase II has developed a structure composed of repeats of a 7 amino-acid sequence. In humans this structure – termed “carboxyterminal domain” or CTD – is composed of 52 such repeats. It is placed exactly at the position where RNA emerges from RNA polymerase II. In less complex organisms the CTD is much shorter: a worm has 36 repeats, and yeast as few as 26, but many single-cell organisms and bacteria have never developed an obvious CTD structure.
Although the requirement of CTD for the expression of cellular genes in higher organisms is undisputed, the molecular details for the gene-specific maturation of RNAs is still largely enigmatic. Research groups have now shown a differential requirement for phosphorylation of the amino acid serine at position 7 of CTD in the processing and maturation of specific gene products.
These results provide the groundwork for the discovery of further pieces of the CTD puzzle and thus enlarge our knowledge of gene regulation. Given its fundamental importance, understanding the mechanism of gene regulation is essential if we are to understand cancer and other diseases at the molecular level and develop new therapies.
Single-Cell Organisms and the Problem of Complexity
Single-cell organisms were already in existence 500 million years ago, with several thousand genes providing different cellular functions. Further developments seemed dependent on producing even more genes.
It would appear that for a highly developed organism like a human, this form of evolution would have resulted in several million genes. But researchers were surprised to learn, following publication of the human genome, that a human only has around 25,000 genes – not many more than a fruit fly or a worm with approximately 15,000 to 20,000 genes.
It would appear that, over the last 500 million years, other ways to produce highly complex organisms have evolved. Evolution has simply found more efficient ways to use the genes already there. But what could have made this possible?
Is there an answer? Yes - it involves the RNA
New results represent a piece of the puzzle and shed new light on to the purpose of an unusual structure in RNA polymerase II.
They build on earlier observations that gene expression is not just regulated by binding of the enzyme to the gene locus to which it is recruited, but also during the phase of active transcription from DNA into RNA. During this phase, parts of the newly synthesised RNA may be removed and the remaining sequences combined into new RNA message. This ‘splicing’ of RNA occurs during gene transcription, and in extreme cases, can produce RNAs coding for several thousand different proteins from a single gene.
How it Works - The Development of CTD
But what was the development that permitted this advance in gene usage? The RNA polymerase II has developed a structure composed of repeats of a 7 amino-acid sequence. In humans this structure – termed “carboxyterminal domain” or CTD – is composed of 52 such repeats. It is placed exactly at the position where RNA emerges from RNA polymerase II. In less complex organisms the CTD is much shorter: a worm has 36 repeats, and yeast as few as 26, but many single-cell organisms and bacteria have never developed an obvious CTD structure.
Although the requirement of CTD for the expression of cellular genes in higher organisms is undisputed, the molecular details for the gene-specific maturation of RNAs is still largely enigmatic. Research groups have now shown a differential requirement for phosphorylation of the amino acid serine at position 7 of CTD in the processing and maturation of specific gene products.
These results provide the groundwork for the discovery of further pieces of the CTD puzzle and thus enlarge our knowledge of gene regulation. Given its fundamental importance, understanding the mechanism of gene regulation is essential if we are to understand cancer and other diseases at the molecular level and develop new therapies.
Tuesday, December 18, 2007
Losses Of Long-established Genes Contribute To Human Evolution
Finding: While it is well understood that the evolution of new genes leads to adaptations that help species survive, gene loss may also afford a selective advantage. A group of scientists has investigated this less-studied idea, carrying out the first systematic computational analysis to identify long-established genes that have been lost across millions of years of evolution leading to the human species.
The idea that gene losses might contribute to adaptation has been kicked around, but not well studied.
To find gene losses a software program called TransMap. The program compared the mouse and human genomes, searching for genes having changes significant enough to render them nonfunctional somewhere during the 75 million years since the divergence of the mouse and the human.
Genes can be lost in many ways. This study focused on losses caused by mutations that disrupt the open reading frame (ORF-disrupting mutations). These are either point mutations, where events such as the insertion or substitution of a DNA base alter the instructions delivered by the DNA, or changes that occur when a large portion of a gene is deleted altogether or moves to a new place on the genome.
Using the Dog Genome
The dog genome was used as an out-group to filter out false positives because the dog diverged from our ancient common ancestor earlier than the mouse. So if a gene is still living in both dog and mouse but not in human, it was probably living in the common ancestor and then lost in the human lineage.
Using this process, they identified 26 losses of long-established genes, including 16 that were not previously known.
The gene loss candidates found in the study do not represent a complete list of gene losses of long-established genes in the human lineage, because the analysis was designed to produce more false negatives than false positives.
The study compares multiple genomes
Next they compared the identified genes in the complete genomes of the human, chimpanzee, rhesus monkey, mouse, rat, dog, and opossum to estimate the amount of time the gene was functional before it was lost. This refined the timing of the gene loss and also served as a benchmark for whether the gene in question was long-established, and therefore probably functional, or merely a loss of a redundant gene copy. Through this process, they found 6 genes that were lost only in the human.
The ACYL3 Protein - A loss From many to none
One previously unknown loss, the gene for acyltransferase-3 (ACYL3), was particularly important. This is an ancient protein that exists throughout the whole tree of life. Multiple copies of the ACYL3 gene are encoded in the fly and worm genomes. In the mammalian clade there is only one copy left, and somewhere along primate evolution, that one copy was lost to the primate clan.
Next it was found that this gene contains a nonsense mutation in both human and chimp, and it appears to still look functional in rhesus. Further, they found that the mutation is not present in the orangutan, so the gene is probably still functional in that species. On the evolutionary tree leading to human, on the branch between chimp and orangutan sits gorilla. Knowing if the gene was still active in gorilla would narrow down the timing of the loss.
The gorilla DNA sequence showed the gene intact, without the mutation, so the loss likely occurred between the speciation of gorilla and chimpanzee.
Other Functional Losses
Acyltransferase-3 was not the only lost gene that doesn't have any close functional homologues in the human genome. A highlight of the research was that they were able to find a list of these orphan losses. Some of them have been functional for more than 300 million years, and they were the last copies left in the human genome. While the copies of these genes remaining in the human genome appear to be nonfunctional, functional copies of all of them exist in the mouse genome.
These orphan genes may be interesting candidates for experimental biologists to explore. It will be interesting to find out what was the biological effect of these losses. Once their function is well characterized in species that still have active copies, we could maybe speculate about their effects on human evolution.
The idea that gene losses might contribute to adaptation has been kicked around, but not well studied.
To find gene losses a software program called TransMap. The program compared the mouse and human genomes, searching for genes having changes significant enough to render them nonfunctional somewhere during the 75 million years since the divergence of the mouse and the human.
Genes can be lost in many ways. This study focused on losses caused by mutations that disrupt the open reading frame (ORF-disrupting mutations). These are either point mutations, where events such as the insertion or substitution of a DNA base alter the instructions delivered by the DNA, or changes that occur when a large portion of a gene is deleted altogether or moves to a new place on the genome.
Using the Dog Genome
The dog genome was used as an out-group to filter out false positives because the dog diverged from our ancient common ancestor earlier than the mouse. So if a gene is still living in both dog and mouse but not in human, it was probably living in the common ancestor and then lost in the human lineage.
Using this process, they identified 26 losses of long-established genes, including 16 that were not previously known.
The gene loss candidates found in the study do not represent a complete list of gene losses of long-established genes in the human lineage, because the analysis was designed to produce more false negatives than false positives.
The study compares multiple genomes
Next they compared the identified genes in the complete genomes of the human, chimpanzee, rhesus monkey, mouse, rat, dog, and opossum to estimate the amount of time the gene was functional before it was lost. This refined the timing of the gene loss and also served as a benchmark for whether the gene in question was long-established, and therefore probably functional, or merely a loss of a redundant gene copy. Through this process, they found 6 genes that were lost only in the human.
The ACYL3 Protein - A loss From many to none
One previously unknown loss, the gene for acyltransferase-3 (ACYL3), was particularly important. This is an ancient protein that exists throughout the whole tree of life. Multiple copies of the ACYL3 gene are encoded in the fly and worm genomes. In the mammalian clade there is only one copy left, and somewhere along primate evolution, that one copy was lost to the primate clan.
Next it was found that this gene contains a nonsense mutation in both human and chimp, and it appears to still look functional in rhesus. Further, they found that the mutation is not present in the orangutan, so the gene is probably still functional in that species. On the evolutionary tree leading to human, on the branch between chimp and orangutan sits gorilla. Knowing if the gene was still active in gorilla would narrow down the timing of the loss.
The gorilla DNA sequence showed the gene intact, without the mutation, so the loss likely occurred between the speciation of gorilla and chimpanzee.
Other Functional Losses
Acyltransferase-3 was not the only lost gene that doesn't have any close functional homologues in the human genome. A highlight of the research was that they were able to find a list of these orphan losses. Some of them have been functional for more than 300 million years, and they were the last copies left in the human genome. While the copies of these genes remaining in the human genome appear to be nonfunctional, functional copies of all of them exist in the mouse genome.
These orphan genes may be interesting candidates for experimental biologists to explore. It will be interesting to find out what was the biological effect of these losses. Once their function is well characterized in species that still have active copies, we could maybe speculate about their effects on human evolution.
Friday, November 23, 2007
Gene comparison between Human and mammals
Finding: By comparing portions of the human genome with those of other mammals, researchers have discovered almost 300 previously unidentified human genes, and found extensions of several hundred genes already known.
Behind the discovery
The fundamental is the idea that as organisms evolve, sections of genetic code that do something useful for the organism change in different ways.
What is the human genome?
The complete sequence of the human genome was accomplished several years ago. That means that the 3 billion or so chemical units, called bases, that make up the order of the genetic code is known. What is not known is the identification of the exact location of all the short sections that code for proteins or perform regulatory or other functions.
The genes make proteins...the basic chemical component needed for building cells. More than 20,000 protein-coding genes have been identified. This finding is important because it shows there still could be many more genes that have been missed using current biological methods. These existing methods are very effective at finding genes that have a wide expression but may miss those that are expressed only in certain tissues or at early stages of embryonic development.
Using evolution for gene discovery
This method involves using evolution to identify these genes. Gene comparision follows evolution; it has been doing this experiment for millions of years. There are many similarities between genes of the two species. The differences can be identified. Using a computer is the microscope to observe the results.
Four different bases -- commonly referred to by the letters G, C, A and T -- make up DNA. Three bases in a row can code for an amino acid (the building blocks of proteins), and a string of these three-letter codes can be a gene, coding for a string of amino acids that a cell can make into a protein.
Conserved genes
Siepel and colleagues set out to find genes that have been "conserved" -- that are fundamental to all life and that have stayed the same, or nearly so, over millions of years of evolution.
The researchers started with "alignments" discovered by other workers -- stretches up to several thousand bases long that are mostly alike across two or more species.
Over millions of years, individual bases can be swapped -- C to G, T to A, for example -- by damage or miscopying. Changes that alter the structure of a protein can kill the organism or send it down a dead-end evolutionary path. But conserved genes contain only minor changes that leave the protein able to do its job. The computer looked for regions with those sorts of changes by creating a mathematical model of how the gene might have changed, then looking for matches to this model.
Behind the discovery
The fundamental is the idea that as organisms evolve, sections of genetic code that do something useful for the organism change in different ways.
What is the human genome?
The complete sequence of the human genome was accomplished several years ago. That means that the 3 billion or so chemical units, called bases, that make up the order of the genetic code is known. What is not known is the identification of the exact location of all the short sections that code for proteins or perform regulatory or other functions.
The genes make proteins...the basic chemical component needed for building cells. More than 20,000 protein-coding genes have been identified. This finding is important because it shows there still could be many more genes that have been missed using current biological methods. These existing methods are very effective at finding genes that have a wide expression but may miss those that are expressed only in certain tissues or at early stages of embryonic development.
Using evolution for gene discovery
This method involves using evolution to identify these genes. Gene comparision follows evolution; it has been doing this experiment for millions of years. There are many similarities between genes of the two species. The differences can be identified. Using a computer is the microscope to observe the results.
Four different bases -- commonly referred to by the letters G, C, A and T -- make up DNA. Three bases in a row can code for an amino acid (the building blocks of proteins), and a string of these three-letter codes can be a gene, coding for a string of amino acids that a cell can make into a protein.
Conserved genes
Siepel and colleagues set out to find genes that have been "conserved" -- that are fundamental to all life and that have stayed the same, or nearly so, over millions of years of evolution.
The researchers started with "alignments" discovered by other workers -- stretches up to several thousand bases long that are mostly alike across two or more species.
Over millions of years, individual bases can be swapped -- C to G, T to A, for example -- by damage or miscopying. Changes that alter the structure of a protein can kill the organism or send it down a dead-end evolutionary path. But conserved genes contain only minor changes that leave the protein able to do its job. The computer looked for regions with those sorts of changes by creating a mathematical model of how the gene might have changed, then looking for matches to this model.
Thursday, November 15, 2007
Evolution Is Deterministic, Not Random -- Multi-species Study
Finding: Biologists in an international team have concluded that developmental evolution is deterministic and orderly, an not the random sequence operation many previously believed based on a study of different species of roundworms.
If organs do not change, how does evolutionary development work in those organs?
Enter the study involving the female copulatory and egg-laying organ, the vulva, found in nearly 50 species of roundworms. The conventional wisdom is that because the vulva does not significantly change across species, one might predict that there would be little variation in vulva development. But that is not the case. Researchers found a lot of developmental variation. They concluded that this variation, since it did not affect the final adult vulva, could not have evolved in a random, fashion.
The research team looked at more than 40 characteristics of vulva development, including cell death, cell division patterns, and related aspects of gonad development. They plotted the evolution of these traits on a new phylogenetic tree, which illustrates how species are related to one another and provides a map as to how evolutionary changes are occurring.
Unidirectional changes
Their results showed an even greater number of evolutionary changes in vulva development than they had expected. But they found that evolutionary changes among these species were unidirectional in nearly all instances.
The decline of cell divisions
For example, they concluded that the number of cell divisions needed in vulva development declined over time instead of randomly increasing and decreasing.
The decline of number of rings
In addition the number of rings used to form the vulva consistently declined during the evolutionary process.
These results demonstrate that, even where you might expect evolution to be random, it is not.
Monday, October 15, 2007
Duplication and Division of Labor - The Mechanics of Evolution
Finding: Evolution works by gene duplication and division of labor.Researchers at the University of Wisconsin-Madison have provided an exquisitely detailed picture of natural selection as it occurs at the genetic level.
Two scientists document how, over many generations, a single yeast gene divides in two and parses its responsibilities to be a more efficient denizen of its environment. The work illustrates, at the most basic level, the driving force of evolution.
This is how new capabilities arise and new functions evolve. This is what goes on in butterflies and elephants and humans. It is evolution in action.
The work is important because it provides the most fundamental view of how organisms change to better adapt to their environments. It documents the workings of natural selection, the critical idea first posited by Charles Darwin where organisms accumulate random variations, and changes that enhance survival are "selected" by being genetically transmitted to future generations.
The new study replayed a set of genetic changes that occurred in a yeast 100 million or so years ago when a critical gene was duplicated and then divided its nutrient processing responsibilities to better utilize the sugars it depends on for food.
One source of newness is gene duplication
When you have two copies of a gene, useful mutations can arise that allow one or both genes to explore new functions while preserving the old function. This phenomenon is going on all the time in every living thing. Many of us are walking around with duplicate genes we're not aware of. They come and go.
Two genes can be better than one because redundancy promotes a division of labor. Genes may do more than one thing, and duplication adds a new genetic resource that can share the workload or add new functions. For example, in humans the ability to see color requires different molecular receptors to discriminate between red and green, but both arose from the same vision gene.
The difficulty, he says, in seeing the steps of evolution is that in nature genetic change typically occurs at a snail's pace, with very small increments of change among the chemical base pairs that make up genes accumulating over thousands to millions of years.
To measure such small change requires a model organism like simple brewer's yeast that produces a lot of offspring in a relatively short period of time. Yeast, Carroll argues, are perfect because their reproductive qualities enable study of genetic change at the deepest level and greatest resolution because researchers can produce and quickly count a large number of organisms. The same work in fruit flies, one of biology's most powerful models, would require "a football stadium full of flies" and years of additional work, Carroll explains.
The process of becoming better occurs in very small steps. When compounded over time, these very small changes make one group of organisms successful and they out-compete others.
The new study involved swapping out different regions of the yeast genome to assess their effects on the performance of the twin genes, as well as engineering in the gene from another species of yeast that had retained only a single copy.
Retracing the Steps of evolution
The work shows in great detail how the ancestral gene gained efficiency through duplication and division of labor. They became optimally connected in that job. They're working in cahoots, but together they are better at the job the ancestral gene held. Natural selection has taken one gene with two functions and sculpted an assembly line with two specialized genes.
Sunday, October 7, 2007
Science and Falseability
Science works on several principles. The most important is the search for truth. The duplication of experiments to verify a claim as true. But also is the possibility of showing that something that is claimed to be true is actually false. That is the falsibility criteria. Here are some examples:The Ptolemaic system of astronomy made some very important claims about how the solar system was structured. That Earth was the center of the solar system...maybe even the universe. It claimed that the stars and the planets orbited around the Earth.
These were scientific claims and as such were subject to verification. As astronomers grew interested in the stars, they becan to examine these claims. Leonardo Da Vince, Gallileo, Kepler, Copernicus, Tyco Brahe and Issac Newton were scientists that researched and found that these claims were false. The earth was not the center of the solar system, the sun was.
The claim was falsifiable. That was important. As a scientific claim it was wrong. It was shown to be wrong, and several astronomers, physicists, and mathematicians were able to verify the experiments that showed how the claim was false, and a new claim was true.
This is the essence of science.
Can the same be said about Evolution? Can it be shown to be falsifiable? This is a critical claim. Because if it cannot be falsifiable then it is like Intelligent Design, a philosophical claim that cannot be verified, or denied.
One way to show that evolution is false would be to show that there are no variations in the human or animal kingdom. But that is not the case. Just recently there was a sad case of an Indian girl that was born with four arms and four legs. This example shows that there are genetic variations possible. But there have to be other tests to show that evolution works. Evolution as a function of genetic mutation.
One experiment would be to expose cells to radiation. If there are no genetic mutations as a result of the experiment then genetic mutation might be suspect as a vehicle of evolution. But as it is there are many cases of radiation leading to genetic mutation. This however is the falsifiability condition.
Tuesday, September 18, 2007
New Method Can Reveal Ancestry Of All Genes Across Many Different Genomes
Finding: A new method has been developed that can reveal the ancestry of all genes across many different genomes. First applied to 17 species of fungi, the approach has unearthed some surprising clues about why new genes pop up in the first place and the biological nips and tucks that bolster their survival.
The problem
The wheels of evolution turn on genetic innovation as new genes with new functions appear, allowing organisms to grow and adapt in new ways. But deciphering the history of how and when various genes appeared, for any organism, has been a difficult and largely intractable task. Having the ability to trace the history of genes on a genomic scale opens the doors to a vast array of interesting and largely unexplored scientific questions. Although the principles laid out in the study pertain to fungi, they could have relevance to a variety of other species as well.
What we know
It has been recognized for decades that new genes first arise as carbon copies of existing genes. It is thought that this replication allows one of the gene copies to persist normally, while giving the other the freedom to acquire novel biological functions. Though the importance of this so-called gene duplication process is well appreciated it is the grist for the mill of evolutionary change the actual mechanics have remained murky, in part because scientists have lacked the tools to study it systematically.
Genes from 17 different species
Driven by the recent explosion of whole genome sequence data, the authors of the new study were able to assemble a natural history of more than 100,000 genes belonging to a group of fungi known as the Ascomycota. From this, the researchers gained a detailed view of gene duplication across the genomes of 17 different species of fungi, including the laboratory model Saccharomyces cerevisiae, commonly known as baker's yeast.
Methodology - Synergy
The basis for the work comes from a new method termed "SYNERGY", which first author Ilan Wapinski and his coworkers developed to help them reconstruct the ancestry of each fungal gene.
By tracing a gene's lineage through various species, the method helps determine in which species the gene first arose, and if -- and in what species -- it became duplicated or even lost altogether. SYNERGY draws its strength from the use of multiple types of data, including the evolutionary or "phylogenetic" tree that depicts how species are related to each other, and the DNA sequences and relative positions of genes along the genome.
Perhaps most importantly, the method does not tackle the problem of gene origins in one fell swoop, as has typically been done, but rather breaks it into discrete, more manageable bits. Instead of treating all species at once, SYNERGY first focuses on a pair of the most recently evolved species -- those at the outer branches of the tree -- and works, two-by-two, toward the more ancestral species that comprise the roots.
From this analysis scientists were able to identify a set of core principles that govern gene duplication in fungi. The findings begin to paint a picture of how new genes are groomed over hundreds of millions of years of evolution.
The problem
The wheels of evolution turn on genetic innovation as new genes with new functions appear, allowing organisms to grow and adapt in new ways. But deciphering the history of how and when various genes appeared, for any organism, has been a difficult and largely intractable task. Having the ability to trace the history of genes on a genomic scale opens the doors to a vast array of interesting and largely unexplored scientific questions. Although the principles laid out in the study pertain to fungi, they could have relevance to a variety of other species as well.
What we know
It has been recognized for decades that new genes first arise as carbon copies of existing genes. It is thought that this replication allows one of the gene copies to persist normally, while giving the other the freedom to acquire novel biological functions. Though the importance of this so-called gene duplication process is well appreciated it is the grist for the mill of evolutionary change the actual mechanics have remained murky, in part because scientists have lacked the tools to study it systematically.
Genes from 17 different species
Driven by the recent explosion of whole genome sequence data, the authors of the new study were able to assemble a natural history of more than 100,000 genes belonging to a group of fungi known as the Ascomycota. From this, the researchers gained a detailed view of gene duplication across the genomes of 17 different species of fungi, including the laboratory model Saccharomyces cerevisiae, commonly known as baker's yeast.
Methodology - Synergy
The basis for the work comes from a new method termed "SYNERGY", which first author Ilan Wapinski and his coworkers developed to help them reconstruct the ancestry of each fungal gene.
By tracing a gene's lineage through various species, the method helps determine in which species the gene first arose, and if -- and in what species -- it became duplicated or even lost altogether. SYNERGY draws its strength from the use of multiple types of data, including the evolutionary or "phylogenetic" tree that depicts how species are related to each other, and the DNA sequences and relative positions of genes along the genome.
Perhaps most importantly, the method does not tackle the problem of gene origins in one fell swoop, as has typically been done, but rather breaks it into discrete, more manageable bits. Instead of treating all species at once, SYNERGY first focuses on a pair of the most recently evolved species -- those at the outer branches of the tree -- and works, two-by-two, toward the more ancestral species that comprise the roots.
From this analysis scientists were able to identify a set of core principles that govern gene duplication in fungi. The findings begin to paint a picture of how new genes are groomed over hundreds of millions of years of evolution.
Sunday, August 26, 2007
One Species, Many Genomes
Finding: Adaptation to the environment may produce many genomes for the same species
Adaptation to the environment has a stronger effect on the genome than anticipated. Faster growth, darker leaves, a different way of branching - wild varieties of the plant Arabidopsis thaliana are often substantially different from the laboratory strain of this small mustard plant, a favorite of many plant biologists.
Discovering which detailed differences distinguish the genomes of strains from the polar circle or the subtropics, from America, Africa or Asia is being investigated for the first time by research teams from Tübingen, Germany, and California. The results were surprising: The extent of the genetic differences far exceeds the expectations for such a streamlined genome, as the scientists write in Science magazine.
To track down the variation in the genome of the different Arabidopsis strains, the researchers compared the genetic material of 19 wild strains with that of the genome of the lab strain, which was sequenced in the year 2000. Using a very elaborate procedure, they examined every one of the roughly 120 million building blocks of the genome.
For their molecular sleuthing they used almost one billion specially designed DNA probes. The result of this painstaking analysis: on average, every 180th DNA building block is variable. And about four percent of the reference genome either looks very different in the wild varieties, or cannot be found at all. Almost every tenth gene was so defective that it could not fulfill its normal function anymore!
From one - many
Results such as these raise fundamental questions. For one, they qualify the value of the model genomes sequenced so far. There isn’t such a thing as the genome of a species. The insight that the DNA sequence of a single individual is by far not sufficient to understand the genetic potential of a species also fuels current efforts in human genetics.
Still, it is surprising that Arabidopsis has such a plastic genome. In contrast to the genome of humans or many crop plants such as corn, that of Arabidopsis is very much streamlined, and its size is less than a twentieth of that of humans or corn—even though it has about the same number of genes. In contrast to these other genomes, there are few repeats or seemingly irrelevant filler sequences. That even in a minimal genome every tenth gene is dispensable, has been a great surprise.
What does the analysis show?
Detailed analyses showed that genes for basic cellular functions such as protein production or gene regulation rarely suffer knockout hits. Genes that are important for the interaction with other organisms, on the other hand, such as those responsible for defense against pathogens or infections, are much more variable than the average gene. The genetic variability appears to reflect adaptation of local circumstances. It is likely that such variable genes allow plants to withstand dry or wet, hot or cold conditions, or make use of short and long growing seasons.
Such genome analyses of unprecedented details will allow a much better understanding of local adaptation, and this was indeed one of the main reasons for conduction the study. By extending these types of studies to other species we hope to help breeders to produce varieties that are optimally adapted to rapidly changing environmental conditions.
New methods - Direct Sequencing
Discovering which detailed differences distinguish the genomes of strains from the polar circle or the subtropics, from America, Africa or Asia is being investigated for the first time by research teams from Tübingen, Germany, and California. The results were surprising: The extent of the genetic differences far exceeds the expectations for such a streamlined genome, as the scientists write in Science magazine.
To track down the variation in the genome of the different Arabidopsis strains, the researchers compared the genetic material of 19 wild strains with that of the genome of the lab strain, which was sequenced in the year 2000. Using a very elaborate procedure, they examined every one of the roughly 120 million building blocks of the genome.
For their molecular sleuthing they used almost one billion specially designed DNA probes. The result of this painstaking analysis: on average, every 180th DNA building block is variable. And about four percent of the reference genome either looks very different in the wild varieties, or cannot be found at all. Almost every tenth gene was so defective that it could not fulfill its normal function anymore!
From one - many
Results such as these raise fundamental questions. For one, they qualify the value of the model genomes sequenced so far. There isn’t such a thing as the genome of a species. The insight that the DNA sequence of a single individual is by far not sufficient to understand the genetic potential of a species also fuels current efforts in human genetics.
Still, it is surprising that Arabidopsis has such a plastic genome. In contrast to the genome of humans or many crop plants such as corn, that of Arabidopsis is very much streamlined, and its size is less than a twentieth of that of humans or corn—even though it has about the same number of genes. In contrast to these other genomes, there are few repeats or seemingly irrelevant filler sequences. That even in a minimal genome every tenth gene is dispensable, has been a great surprise.
What does the analysis show?
Detailed analyses showed that genes for basic cellular functions such as protein production or gene regulation rarely suffer knockout hits. Genes that are important for the interaction with other organisms, on the other hand, such as those responsible for defense against pathogens or infections, are much more variable than the average gene. The genetic variability appears to reflect adaptation of local circumstances. It is likely that such variable genes allow plants to withstand dry or wet, hot or cold conditions, or make use of short and long growing seasons.
Such genome analyses of unprecedented details will allow a much better understanding of local adaptation, and this was indeed one of the main reasons for conduction the study. By extending these types of studies to other species we hope to help breeders to produce varieties that are optimally adapted to rapidly changing environmental conditions.
New methods - Direct Sequencing
How environment and genome interact is also the goal of new methods. While the technology used so far can only identify genes that have changed or are lost relative to the reference genome, direct sequencing of the genome of wild strains will allow the detection of new genes. The plan is to decipher the genomes of at least 1001 Arabidopsis varieties. A new instrument, with which the entire genome of a plant can be read in just a few days, is already available. Still missing are the computational algorithms to interpret the anticipated flood of data.
Sunday, August 19, 2007
Genes changes linked to an organism's survivability
Studies from biologists have found that a simple interaction between just two genes determines the patterns of fur coloration that camouflage mice against their background, protecting them from many predators. The work marks one of the few instances in which specific genetic changes have been linked to an organism's ability to survive in the wild.
What does the research show?
The work shows how changes in just a few genes can greatly alter an organism's appearance. It also illuminates the pathway by which these two genes interact to produce distinctive coloration. The result is that now there's reason to believe this simple pathway may be evolutionarily conserved across mammals that display lighter bellies and darker backs, from mice to tuxedo cats to German Shepherds.
What was studied?
Researchers studied Peromyscus, a mouse that is the most widespread mammal in North America. Within the last several thousand years, these mice have migrated from mainland Florida to barrier islands and dunes along the Atlantic and Gulf coasts, where they now live on white sand beaches. In the process, the beach mice's coats have become markedly lighter than that of their mainland brethren.
What did the research show?
Nature provides a tremendous amount of variation in color patterns among organisms, ranging from leopard spots to zebra stripes; these patterns help individuals survive. But it has been difficult to understand how these adaptive color patterns are generated. The research helped identify the genetic changes producing a simple color pattern that helps camouflage mice inhabiting the sandy dunes of Florida's Gulf and Atlantic coasts. These 'beach mice' have evolved a lighter pigmentation than their mainland relatives, a coloration that helps camouflage them from predators that include owls, herons, and hawks.
Previous research has shown that such predators, all of which hunt by sight, will preferentially catch darker mice on the white sand beaches, providing a powerful opportunity for natural selection to evolve increased camouflage.
Which Genes were involved?
Through a detailed genomic analysis, researchers identified two pigmentation genes, for the melanocortin-1 receptor (Mc1r) and an agouti signaling protein (Agouti) that binds to this receptor and turns it off. Conclusion: A single amino-acid mutation in Mc1r gene can weaken the receptor's activity, or a mutation in the Agouti gene can increase the amount of protein present without changing the protein's sequence, also reducing Mc1r activity and yielding lighter pigmentation.
Research findings
What do the genes do? Both genes affect the type and amount of melanin in individual hairs. If both genes are turned on, the mouse is dark in color. If a mutation occurs, which changes either gene this leads to a somewhat blonder mouse, but when the combination of mutations occur in both genes this produces a mouse very light in color.
What does the research show?
The work shows how changes in just a few genes can greatly alter an organism's appearance. It also illuminates the pathway by which these two genes interact to produce distinctive coloration. The result is that now there's reason to believe this simple pathway may be evolutionarily conserved across mammals that display lighter bellies and darker backs, from mice to tuxedo cats to German Shepherds.
What was studied?
Researchers studied Peromyscus, a mouse that is the most widespread mammal in North America. Within the last several thousand years, these mice have migrated from mainland Florida to barrier islands and dunes along the Atlantic and Gulf coasts, where they now live on white sand beaches. In the process, the beach mice's coats have become markedly lighter than that of their mainland brethren.
What did the research show?
Nature provides a tremendous amount of variation in color patterns among organisms, ranging from leopard spots to zebra stripes; these patterns help individuals survive. But it has been difficult to understand how these adaptive color patterns are generated. The research helped identify the genetic changes producing a simple color pattern that helps camouflage mice inhabiting the sandy dunes of Florida's Gulf and Atlantic coasts. These 'beach mice' have evolved a lighter pigmentation than their mainland relatives, a coloration that helps camouflage them from predators that include owls, herons, and hawks.
Previous research has shown that such predators, all of which hunt by sight, will preferentially catch darker mice on the white sand beaches, providing a powerful opportunity for natural selection to evolve increased camouflage.
Which Genes were involved?
Through a detailed genomic analysis, researchers identified two pigmentation genes, for the melanocortin-1 receptor (Mc1r) and an agouti signaling protein (Agouti) that binds to this receptor and turns it off. Conclusion: A single amino-acid mutation in Mc1r gene can weaken the receptor's activity, or a mutation in the Agouti gene can increase the amount of protein present without changing the protein's sequence, also reducing Mc1r activity and yielding lighter pigmentation.
Research findings
What do the genes do? Both genes affect the type and amount of melanin in individual hairs. If both genes are turned on, the mouse is dark in color. If a mutation occurs, which changes either gene this leads to a somewhat blonder mouse, but when the combination of mutations occur in both genes this produces a mouse very light in color.
Sunday, August 5, 2007
Genetic Chromosome Breaking
Researchers in genome stability have observed that many kinds of cancer are associated with areas where human chromosomes break. Its been hypothesized, but not proven, that slow or altered replication led to the chromosomes breaking.
But now a study at Tufts University two molecular biologists have used yeast artificial chromosomes to prove that hypothesis. They found a highly flexible DNA sequence that increases fragility and stalls replication, which then causes the chromosome to break.
Cancer Causing Areas
The area in question is an area that has a tumor suppressor gene -- a gene whose absence can cause tumors. If you delete that gene or delete part of that gene so it doesn't work anymore, that can lead to tumors. The fact that there is fragility in the same region that this gene is located is a bad coincidence. Fragility can cause deletions and deletions can cause cancer, so you want to understand the fragility because that might be what's causing cancer.
DNA structure leads to fragility
Past research had predicted the flexibility of the DNA helix in this particular common fragile site by calculating the twist angle between consecutive base pairs and found that there were several points of high flexibility, suggesting that the flexibility was connected to the fragility.
Freudenreich and Zhang used yeast artificial chromosomes to test this idea because it allowed them to look at the region in a more detailed way than looking at human chromosomes and to monitor the replication process. They expect the results will be similar when tested in human cells based on previous research using yeast chromosomes.
How the research was conducted
Two regions of predicted high flexibility, plus a region near a cancer cell breakpoint and a control region were tested to see whether any of these regions could cause breakage of a yeast chromosome. They found that one did. This is the first known sequence element within a human common fragile site shown to increase chromosome breakage. What is intriguing is that the sequence that breaks, in addition to being flexible, is predicted to form an abnormal DNA structure." The result is that when replication stalls, chromosomes can break.
How did the chromosomes break?
From past studies, they hypothesized that breakage was connected to replication. Replication is just the duplication of DNA in side the cells as they divide, the DNA inside those cells must duplicate. The research showed that the chromosomes were breaking because replication was stalled.
The problem arises when they do not heal correctly and instead are deleted or rearranged, Cancer cells almost always have some sort of deletions or rearrangements. Something is wrong with their chromosomes that then messes up the genes that are in those areas.
Replication process stalled
The researchers also noticed that this particular sequence was an AT-rich region, where the DNA was composed mostly of the bases adenine (A) and thymine (T), rather than the other bases cytosine (C) or guanine (G). Freudenreich and Zhang found the longer the AT-repeat, the more the replication process was stalled, something they would like to follow up on with further research.
Some researchers believe that the longer the repeat, the more the abnormal the DNA structure forms, and the more fragile the chromosome becomes. What is still up in the air is whether people with longer repeats are more prone to deleting that tumor suppressor gene and getting cancer as a result. Does this correlation between chromosome breaks and cancer has a medical consequence.
But now a study at Tufts University two molecular biologists have used yeast artificial chromosomes to prove that hypothesis. They found a highly flexible DNA sequence that increases fragility and stalls replication, which then causes the chromosome to break.
Cancer Causing Areas
The area in question is an area that has a tumor suppressor gene -- a gene whose absence can cause tumors. If you delete that gene or delete part of that gene so it doesn't work anymore, that can lead to tumors. The fact that there is fragility in the same region that this gene is located is a bad coincidence. Fragility can cause deletions and deletions can cause cancer, so you want to understand the fragility because that might be what's causing cancer.
DNA structure leads to fragility
Past research had predicted the flexibility of the DNA helix in this particular common fragile site by calculating the twist angle between consecutive base pairs and found that there were several points of high flexibility, suggesting that the flexibility was connected to the fragility.
Freudenreich and Zhang used yeast artificial chromosomes to test this idea because it allowed them to look at the region in a more detailed way than looking at human chromosomes and to monitor the replication process. They expect the results will be similar when tested in human cells based on previous research using yeast chromosomes.
How the research was conducted
Two regions of predicted high flexibility, plus a region near a cancer cell breakpoint and a control region were tested to see whether any of these regions could cause breakage of a yeast chromosome. They found that one did. This is the first known sequence element within a human common fragile site shown to increase chromosome breakage. What is intriguing is that the sequence that breaks, in addition to being flexible, is predicted to form an abnormal DNA structure." The result is that when replication stalls, chromosomes can break.
How did the chromosomes break?
From past studies, they hypothesized that breakage was connected to replication. Replication is just the duplication of DNA in side the cells as they divide, the DNA inside those cells must duplicate. The research showed that the chromosomes were breaking because replication was stalled.
The problem arises when they do not heal correctly and instead are deleted or rearranged, Cancer cells almost always have some sort of deletions or rearrangements. Something is wrong with their chromosomes that then messes up the genes that are in those areas.
Replication process stalled
The researchers also noticed that this particular sequence was an AT-rich region, where the DNA was composed mostly of the bases adenine (A) and thymine (T), rather than the other bases cytosine (C) or guanine (G). Freudenreich and Zhang found the longer the AT-repeat, the more the replication process was stalled, something they would like to follow up on with further research.
Some researchers believe that the longer the repeat, the more the abnormal the DNA structure forms, and the more fragile the chromosome becomes. What is still up in the air is whether people with longer repeats are more prone to deleting that tumor suppressor gene and getting cancer as a result. Does this correlation between chromosome breaks and cancer has a medical consequence.
Thursday, August 2, 2007
Genetic Factors Strongly Shape How Peers Are Chosen
The company we keep may be more influenced by genetics than previously thought. Researchers report that as individuals develop, genes become more important in influencing how they choose their peer groups. The findings offer insight into which individuals may be at risk for future substance use or other externalizing behaviors such as conduct and antisocial personality disorder.
The study involved 1,800 male twin pairs from mid-childhood to early adulthood, between 1998 and 2004.
Through a series of interviews, researchers found that genetic factors increasingly impact how male twins make choices as they mature and develop their own social groups. Their finding include that the path from genes to behaviors like drug use and antisocial behaviors is not entirely direct or biological. Rather an important part of this pathway involves the genetics, which influences our own social environment, which in turn impacts on our risk for a whole host of deviant behaviors. Results demonstrate clearly that a complete understanding of the pathway from genes to antisocial behaviors, including drug abuse, has to take into account self-selection into deviant versus benign environments. The effects of peers in adolescence can be quite powerful, either encouraging or discouraging deviant behaviors. Peers also provide access to substances of abuse.
The study involved 1,800 male twin pairs from mid-childhood to early adulthood, between 1998 and 2004.
Through a series of interviews, researchers found that genetic factors increasingly impact how male twins make choices as they mature and develop their own social groups. Their finding include that the path from genes to behaviors like drug use and antisocial behaviors is not entirely direct or biological. Rather an important part of this pathway involves the genetics, which influences our own social environment, which in turn impacts on our risk for a whole host of deviant behaviors. Results demonstrate clearly that a complete understanding of the pathway from genes to antisocial behaviors, including drug abuse, has to take into account self-selection into deviant versus benign environments. The effects of peers in adolescence can be quite powerful, either encouraging or discouraging deviant behaviors. Peers also provide access to substances of abuse.
Monday, July 30, 2007
Repetitive DNA
Repetitive DNA studies of many organisms has revealed that a large proportion of eukaryotic genomes consists of repetitive DNA.
For example in the kangaroo rat
garbage is stuff you don't want so you throw it away.
These sequences might have some function we don't know about so they have been called junk DNA. The fact that such sequences seem to accumulate in genomes has lead to the notion that repetitive DNA is selfish DNA, since the sequence makes additional copies of itself within the genome decoupled from the reproduction rate of the host.
For example in the kangaroo rat
- the sequence (AAG) is repeated 2.4 billion times,
- the sequence (TTAGGG) is repeated 2.2 billion times and
- the sequence (ACACAGCGGG) is repeated 1.2 billion times.
What it does is unclear. These are called junk DNA sequences.
Note that junk is stuff you don't throw away because it might be useful some day;garbage is stuff you don't want so you throw it away.
These sequences might have some function we don't know about so they have been called junk DNA. The fact that such sequences seem to accumulate in genomes has lead to the notion that repetitive DNA is selfish DNA, since the sequence makes additional copies of itself within the genome decoupled from the reproduction rate of the host.
Sunday, July 29, 2007
The Chloroplast Genome
The genome of the chloroplasts found in Marchantia polymorpha contains 121,024 base pairs in a closed circle.A chloroplast is the organelle that carries out photosynthesis and starch grain formation. It is a chlorophyll-containing organelle in plants that is the site of photosynthesis.
These make up some 128 genes which include:
- duplicate genes encoding each of the four subunits (23S, 16S, 4.5S, and 5S) of the ribosomal RNA (rRNA) used by the chloroplast
- 37 genes encoding all the transfer RNA (tRNA) molecules used for translation within the chloroplast.
Some of these are represented in the figure by black bars.
4 genes encoding some of the subunits of the RNA polymerase used for transcription within the chloroplast (the blue ones)
a gene encoding the large subunit of the enzyme ribulose bisphosphate carboxylase oxygenase (RUBISCO)
9 genes for components of photosystems I and II
6 genes encoding parts of the chloroplast ATP synthase
genes for 19 of the ~60 proteins used to construct the chloroplast ribosome
Saturday, July 28, 2007
The Mitochondrial Genome
What does the genome of human mitochondria look like?It contains 16,569 base pairs of DNA organized in a closed circle.
These encode:
- 2 ribosomal RNA (rRNA) molecules
- 22 transfer RNA (tRNA) molecules (shown in the figure as yellow bars; two of them labeled)
- 13 polypeptides.
The 13 polypeptides participate in building several protein complexes embedded in the inner mitochondrial membrane.
- 7 subunits that make up the mitochondrial NADH dehydrogenase
- 3 subunits of cytochrome c oxidase
- 2 subunits of ATP synthase cytochrome b
Wednesday, July 25, 2007
The Out of Nowhere Gene
New genes have been for decades believed to created from existing genes. New research that some new genes pop up Out of Nowhere. Researchers studying the Drosophilia fruit fly have discovered a gene without peers.
A new gene, called hydra, exists in only a small number of species of Drosophila fruit flies. Research indicates that the gene was created roughly 13 million years ago, when it is believed that the melanogaster subgroup species diverged from a common ancestor.
In addition to the appearance of new gene, some early evidence also shows that this new gene is functional i.e. not "junk" DNA. and may express itself as a protein involved in late stages of sperm cell development (spermatogenesis). Other scientists working with functional genes in any species also are expressed in male testes and appear related to spermatogenesis.
One problem that the researchers are working on is how the hydra gene was created. They believe that it came out of nowhere. Some speculate that the gene may have developed from a piece of DNA junk called a transposable element which some refer to as a "jumping gene". It may have been inserted into the genome by a virus. These transposons are known to copy and insert themselves into DNA sequences. One theory is that when a transposon sits next to a gene it carries part of the gene sequence it was next to and then if it jumps to a new location it inserts that gene sequence in the new location. Current thinking is that transposable gene elements appear to have no function or may be harmful and are eliminated by natural selection, however, other researchers believe that some transposons may be a source for creating new functional genes as well.
A new gene, called hydra, exists in only a small number of species of Drosophila fruit flies. Research indicates that the gene was created roughly 13 million years ago, when it is believed that the melanogaster subgroup species diverged from a common ancestor.
In addition to the appearance of new gene, some early evidence also shows that this new gene is functional i.e. not "junk" DNA. and may express itself as a protein involved in late stages of sperm cell development (spermatogenesis). Other scientists working with functional genes in any species also are expressed in male testes and appear related to spermatogenesis.
One problem that the researchers are working on is how the hydra gene was created. They believe that it came out of nowhere. Some speculate that the gene may have developed from a piece of DNA junk called a transposable element which some refer to as a "jumping gene". It may have been inserted into the genome by a virus. These transposons are known to copy and insert themselves into DNA sequences. One theory is that when a transposon sits next to a gene it carries part of the gene sequence it was next to and then if it jumps to a new location it inserts that gene sequence in the new location. Current thinking is that transposable gene elements appear to have no function or may be harmful and are eliminated by natural selection, however, other researchers believe that some transposons may be a source for creating new functional genes as well.
Tuesday, July 24, 2007
Genetic variation and Genetic stability
Scientists from the Max-Plank institute and from the Salk Institute and the university of Chicago have identified which genes are prone to variation and which are stable and do not have modification. They have developed a method to sift out whole genomes for all the environmental fixes and addendums accumulated over time. What the scientists are after is the regions that are currently targeted by natural selection or have been so during the evolutionary past.
This is an exciting prospect because it lends itself to a further accumulation of evidence about how evolution works. The entire genome isn't affected, only parts of it. Scientists studying the plant the mustard weed Arabidopsis thaliana have been able to identify genetic variations in 23 strains.
Why study arabidopsis?
About 10 years ago Arabidopsis was adopted by plant scientists as an easily manipulated model for other plants because it is simple to grow in the laboratory, has a short life cycle and a small genome. Arabidopsis only has about 120 million base pairs of DNA. Compared to corn, which might have as many as 2.5 billion base pairs of DNA and the human genome with roughly 3 billion pairs, one can study it more easily.
Effects on genes
Plants are under constant threat from heat, cold, high acidity or salinity, or pathogens such as viruses and leaf-munching insects. So how do plants survive? Plants mobilize physiological and biochemical defenses for their survival. Scientists expected certain classes of genes to be highly variable due to natural selection in different environments. And now two different studies revealed precisely which gene family members indeed were shaped by evolution. In general, genes that don't change over time are under strong negative selection because they perform important housekeeping functions, while genes that vary widely such as disease resistance genes are under strong positive selection.
This is an exciting prospect because it lends itself to a further accumulation of evidence about how evolution works. The entire genome isn't affected, only parts of it. Scientists studying the plant the mustard weed Arabidopsis thaliana have been able to identify genetic variations in 23 strains.
Why study arabidopsis?
About 10 years ago Arabidopsis was adopted by plant scientists as an easily manipulated model for other plants because it is simple to grow in the laboratory, has a short life cycle and a small genome. Arabidopsis only has about 120 million base pairs of DNA. Compared to corn, which might have as many as 2.5 billion base pairs of DNA and the human genome with roughly 3 billion pairs, one can study it more easily.
Effects on genes
Plants are under constant threat from heat, cold, high acidity or salinity, or pathogens such as viruses and leaf-munching insects. So how do plants survive? Plants mobilize physiological and biochemical defenses for their survival. Scientists expected certain classes of genes to be highly variable due to natural selection in different environments. And now two different studies revealed precisely which gene family members indeed were shaped by evolution. In general, genes that don't change over time are under strong negative selection because they perform important housekeeping functions, while genes that vary widely such as disease resistance genes are under strong positive selection.
Wednesday, July 4, 2007
The Origins of the domesticated cat
This was a great story I came across. It's about the origin of the domesticated cat. Like many of you, I was under the impression that it was Egypt that domesticated the cat but that notion is wrong.
The domesticated cat came from the Fertile Crescent in the Middle East about 130,000 years ago when wildcats moved into villages. Scientists have discovered five modern genetic lines to the wildcat species. It shows that domestication came from the cats wanting to be with humans. Humans used them for mice patrol; they did not hunt cats, but tolerated them. The work bolsters the notion that cats became useful to humans when agriculture started forcing people to protect grain stores from rodents.
As species go Wildcats are single Old World. And five subspecies lived in Europe, sub-Saharan Africa, China, Central Asia, and the Near East. So researchers collected genetic material from almost a thousand cats, both wild and domestic, from three continents. What they were able to find was that the common ancestors of all domesticated cats lived in the Near East some 130,000 years ago.
The domesticated cat came from the Fertile Crescent in the Middle East about 130,000 years ago when wildcats moved into villages. Scientists have discovered five modern genetic lines to the wildcat species. It shows that domestication came from the cats wanting to be with humans. Humans used them for mice patrol; they did not hunt cats, but tolerated them. The work bolsters the notion that cats became useful to humans when agriculture started forcing people to protect grain stores from rodents.
As species go Wildcats are single Old World. And five subspecies lived in Europe, sub-Saharan Africa, China, Central Asia, and the Near East. So researchers collected genetic material from almost a thousand cats, both wild and domestic, from three continents. What they were able to find was that the common ancestors of all domesticated cats lived in the Near East some 130,000 years ago.
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