2007-01-22
Have a Pingpong Game
"Do you join us to have a pingpong game?"Tonight after finished my experiment, I was invited to have a game. From an exciting and interesting game lasted from 7pm to 10:30, I learned that——Practice makes Perfect!
2007-01-19
Chicken is on-the-fly
Complete Chicken Genome Sequenced
By Sarah Graham
The chicken has joined the growing group of animals whose genome has been sequenced. The findings, published today in the journal Nature, reveal that, like us, the bird has between 20,000 and 23,000 genes. But it has only 1 billion DNA base pairs to our 2.9 billion pairs. "The chicken has also been used extensively as a model by developmental biologists for over a century and the availability of a gene catalogue for the species will boost research in this area," says David Burt of the Roslin Institute in Edinburgh and a member of the International Chicken Genome Sequencing Consortium.
The results indicate that humans share about 60 percent of their genes with the chicken; humans and rats have 88 percent of their genes in common. The reduced number of base pairs in the fowl genome results in part from chickens possessing less so-called junk DNA than humans do. "The recognizable repetitive content of the chicken genome is only about 10 percent as compared to about 50 percent for humans," explains lead author LaDeana Hillier of Washington University School of Medicine. The team also found some unique common ground between people and chickens: for example, there is a chicken gene for interleukin 26, which is an important immune response in people and had not yet been identified in other animals.
The results should help scientists better understand basic developmental biology, as well as improve vaccine production models. "Genomes of the chicken and other species distant from ourselves have provided us with a powerful tool to resolve key biological processes that have been conserved over millennia," comments consortium leader Richard Wilson of Washington State University. "Along with the many similarities between the chicken and human genomes, we discovered some fascinating differences that are shedding new light on what distinguishes birds from mammals."
The Incredible, Medical Egg
Genetically modified chickens that produce medicines in their eggs may be the drug factories of the future
By David Biello
By Sarah Graham
The chicken has joined the growing group of animals whose genome has been sequenced. The findings, published today in the journal Nature, reveal that, like us, the bird has between 20,000 and 23,000 genes. But it has only 1 billion DNA base pairs to our 2.9 billion pairs. "The chicken has also been used extensively as a model by developmental biologists for over a century and the availability of a gene catalogue for the species will boost research in this area," says David Burt of the Roslin Institute in Edinburgh and a member of the International Chicken Genome Sequencing Consortium.
The results indicate that humans share about 60 percent of their genes with the chicken; humans and rats have 88 percent of their genes in common. The reduced number of base pairs in the fowl genome results in part from chickens possessing less so-called junk DNA than humans do. "The recognizable repetitive content of the chicken genome is only about 10 percent as compared to about 50 percent for humans," explains lead author LaDeana Hillier of Washington University School of Medicine. The team also found some unique common ground between people and chickens: for example, there is a chicken gene for interleukin 26, which is an important immune response in people and had not yet been identified in other animals.
The results should help scientists better understand basic developmental biology, as well as improve vaccine production models. "Genomes of the chicken and other species distant from ourselves have provided us with a powerful tool to resolve key biological processes that have been conserved over millennia," comments consortium leader Richard Wilson of Washington State University. "Along with the many similarities between the chicken and human genomes, we discovered some fascinating differences that are shedding new light on what distinguishes birds from mammals."
The Incredible, Medical Egg
Genetically modified chickens that produce medicines in their eggs may be the drug factories of the future
By David Biello
2007-01-14
Too early to bed, too early to rise
interesting! Geneticists track the cause behind early rising and assoaciated it with gene.
News
Published online: 11 January 2007; doi:10.1038/news070108-9
Heidi Ledford
Bed time? For some, 7pm is too late to stay awake.GettySociety celebrates its early birds, but for an unlucky few, the internal alarm clock goes off much too early. Now, studies of early-rising mice have led researchers to change their view of how biological clocks tell time, and could ultimately lead to new treatments for people with sleep disorders.Variation in sleep cycles is normal, says Louis Ptácek, a geneticist at the University of California at San Francisco. "In the general population, there's a huge spectrum between people who habitually wake up without an alarm clock or coffee at 6 am, and those who would sleep until two in the afternoon if they didn't have any other responsibilities," says Ptácek.But at the far reaches of normal behaviour are individuals whose internal curfews are set much earlier or later than those of the rest of the population. People who have familial advanced sleep phase syndrome — which Ptácek estimates affects only 0.3% of the population — usually wake up around 4 in the morning, and go to bed around 7 at night."The time that most people are most awake is around dinnertime," says Ptácek. "But that's when these people are so sleepy that their face could fall into a bowl of soup." Ptácek and his colleagues previously showed that some people with the condition carried a mutation in a gene called period 2 (PER2), and levels of PER2 proteins are often critically low.Researchers previously thought that the mutation associated with this syndrome caused PER2 proteins to degrade. But now, this team's work with affected mice shows that the mutated gene simply makes less protein in the first place. That's a complete reversal in thinking says David Virshup, a biochemist at the University of Utah in Salt Lake City. "It all made perfect sense to us then, and it all makes perfect sense now, but in the opposite direction."The result, published in Cell1, should have implications for those trying to manipulate the body-clock system, perhaps even with a simple pill. Such treatments could be used for many disorders, from serious sleep problems to simple jetlag.Wake me upThe overall picture of body-clock regulation has also become more complicated through this research. The team found that the PER2 gene has two sites that can be modified by a well-known chemical trigger, which is in turn activated by another gene.Only one of these sites is implicated in familial advanced sleep phase syndrome. At this site, the chemical trigger normally increases expression of PER2. But in those with a mutation, the trigger is ineffectual, and PER2 levels start to decline. At the second site, the trigger does the opposite — it degrades the protein.
There is no known human condition associated with a mutation at this second site. But the researchers think that it probably plays a part in the normal body clock, with some unknown regulation system moderating the interactions between the two. "It's sort of a yin-yang type of relationship," says Steve Kay, a body-clock researcher at the Scripps Research Institute in La Jolla, California. "The two sites have to balance each other out to produce the tight clock regulation that we see."Researchers are now chasing down that new regulatory component in the hope that it could one day be used to derive a treatment for people with sleep disorders.
News
Published online: 11 January 2007; doi:10.1038/news070108-9
Heidi Ledford
Bed time? For some, 7pm is too late to stay awake.GettySociety celebrates its early birds, but for an unlucky few, the internal alarm clock goes off much too early. Now, studies of early-rising mice have led researchers to change their view of how biological clocks tell time, and could ultimately lead to new treatments for people with sleep disorders.Variation in sleep cycles is normal, says Louis Ptácek, a geneticist at the University of California at San Francisco. "In the general population, there's a huge spectrum between people who habitually wake up without an alarm clock or coffee at 6 am, and those who would sleep until two in the afternoon if they didn't have any other responsibilities," says Ptácek.But at the far reaches of normal behaviour are individuals whose internal curfews are set much earlier or later than those of the rest of the population. People who have familial advanced sleep phase syndrome — which Ptácek estimates affects only 0.3% of the population — usually wake up around 4 in the morning, and go to bed around 7 at night."The time that most people are most awake is around dinnertime," says Ptácek. "But that's when these people are so sleepy that their face could fall into a bowl of soup." Ptácek and his colleagues previously showed that some people with the condition carried a mutation in a gene called period 2 (PER2), and levels of PER2 proteins are often critically low.Researchers previously thought that the mutation associated with this syndrome caused PER2 proteins to degrade. But now, this team's work with affected mice shows that the mutated gene simply makes less protein in the first place. That's a complete reversal in thinking says David Virshup, a biochemist at the University of Utah in Salt Lake City. "It all made perfect sense to us then, and it all makes perfect sense now, but in the opposite direction."The result, published in Cell1, should have implications for those trying to manipulate the body-clock system, perhaps even with a simple pill. Such treatments could be used for many disorders, from serious sleep problems to simple jetlag.Wake me upThe overall picture of body-clock regulation has also become more complicated through this research. The team found that the PER2 gene has two sites that can be modified by a well-known chemical trigger, which is in turn activated by another gene.Only one of these sites is implicated in familial advanced sleep phase syndrome. At this site, the chemical trigger normally increases expression of PER2. But in those with a mutation, the trigger is ineffectual, and PER2 levels start to decline. At the second site, the trigger does the opposite — it degrades the protein.
There is no known human condition associated with a mutation at this second site. But the researchers think that it probably plays a part in the normal body clock, with some unknown regulation system moderating the interactions between the two. "It's sort of a yin-yang type of relationship," says Steve Kay, a body-clock researcher at the Scripps Research Institute in La Jolla, California. "The two sites have to balance each other out to produce the tight clock regulation that we see."Researchers are now chasing down that new regulatory component in the hope that it could one day be used to derive a treatment for people with sleep disorders.
2007-01-06
Gene Behind Mendel's Green Pea Seeds Finally Identified
SCIENCE NEWS January 05, 2007
More than a century later, researchers isolate a gene manipulated by the Austrian monk in his groundbreaking experiments
By JR Minkel
More than a century later, researchers isolate a gene manipulated by the Austrian monk in his groundbreaking experiments
By JR Minkel
Image: GNU Public License--Rasbak
Pisum sativum: Researchers have identified one of the pea plant genes that monk Gregor Mendel first studied more than a century ago.
Quite Mendelian: Gregor Mendel (1822-1884), the founder of genetics.
It only took 141 years, but researchers report they have finally pinpointed one of the genes that Austrian monk Gregor Mendel manipulated in his pioneering experiments that established the basic laws of genetics--specifically, the gene that controlled the color of his peas' seeds. A team identified the sequence of a gene common to several plant species, which use it to break down a green pigment molecule, and found that it matches Mendel's gene.
This marks the third of the monk's seven genes that researchers have precisely identified, and the first since the late 1990s, before the genome sequencing boom.
"It's extremely gratifying," says plant geneticist Ian Armstead of the Institute of Grassland and Environmental Research in Aberystwyth, Wales, lead author of a report on the findings in this week's Science. "Many of the loci that Mendel looked at haven't been characterized biochemically before, and it's just interesting to have discovered one of them."
If you've ever taken a biology class, you may recall seeing a portrait of Mendel next to a picture of pea plants that vary in traits such as their height and the color and shape of their seeds (round or wrinkled; green or yellow). By counting the proportions of these traits in several generations of pea plants, the inquisitive monk concluded that these features must derive from pairs of what we now call genes, which he discovered were randomly divided between offspring.
But researchers had never managed to sequence Mendel's gene for seed color, and the pea genome is too huge to go fishing for it, says co-author Norman Weeden, a pea researcher at Montana State University. Luckily, along came Armstead and his colleagues, who were working to precisely locate the sequence of a gene called staygreen (sgr) in the meadow grass Festuca pratensis, some variants of which remain green in drought and other unfavorable conditions because they are unable to break down a green pigment.
The key forward was the genetic similarity between Festuca and rice, which has had its genome sequenced. The group compared genetic markers specific to the sgr region of the grass's chromosome with the markers on the corresponding portion of the rice genome.
The rice chromosome contained 30 potential genes in that area, including one similar to other pigment-metabolizing proteins. To confirm the gene's function, the researchers turned to another lab plant, the thale cress Arabidopsis thaliana, in which they could deactivate the corresponding gene; they found that the resulting plants stayed green longer.
To find out if the equivalent pea sgr was Mendel's gene, they picked out the location of its sequence from pea plants that varied in their seed color. Sure enough, the pea version of sgr was always found in the same tiny part of the chromosome as the old monk's seed color gene. "We still don't know exactly how it does what it does," Armstead says, "but now we have the gene and we can begin to study it."
As for the identities of Mendel's other four genes, Weeden says he expects them to be revealed in the next few years as more plant genomes give up their sequences. "I was hoping they'd go a little faster," he says.
from SCIENCE AMERICAN
2007-01-03
Potluck
Had a potluck in my Boss's home: All of his students us went to his home with no cooked food, instead, we were required to show one's own best food with any material bought from the nearby supermarket. My God! He did give a big trouble, because I was not good at kitchen. Certainly, I won't lose the free supper——learn to make a Northestern Luan-Dun(东北乱炖)the easiest dish made up of potato, tomato, pork chop and other vegetable. My boss's wife ,Chen hj,Duan xd,Liao z,Li f,Xiong hp,Zhou X and me were busy with a "big" supper from 2pm to 10pm——imagine it preparing a supper for Spring Festival Eve! Chinese food with France red wine, a beautiful time!
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