positive results

Waiting for a long long time, today, exactly tonight, I got my eagerly expected results--one year after my research project activated! So exciting, so fighting!Thanks for friends and classmates in Lab505, my parents, brothers ………
it's you
encouraged me during my lasting negative results;
it's you
surpported me in my depressing days;
it's you
freshed up me when i'm going to give up;
Thank you all！

deface show

What disgrace!! You can't imagine how embarrassed i was on this seminar!!! Unexpected, in English, a very simple article was distorted to show for group members. I gave a so bad journal introduction on group's journal club; i made a so impressive show for all group members! Sigh... :(
What suggestions i got from my boss and classmates is that i should firstly confer key point of every slides to audience in no more than two sentences. It is not good to try to explain each detailed background information supposing they have known.It is better to speak oral English but formal English.
Yes, there is a going, "Write to be understood, speak to be heard, read to grow."--Lawrence Clark Powell Wish i would a good representation next time.

host a visiting scientist from CSHL

Invited by my boss, a well known scientist from America Cold Spring Harbour Laboratory, Michael Q. Zhang(http://rulai.cshl.edu/ ) visited our lab this afternoon. He gave a speech in Chinese on "Computational dissection of mammalian genome regulation sub networks" and would stay in NJ for several days. What i got from his address remains some key words: promoter- transcription -correlation-dynamic regulation and protein-protein interaction……
upload some photos here

National Day

Busy National Day.
Brett Tyler is professor at the Virginia Bioinformatics Institute and at the Department of Plant Pathology, Physiology and Weed Science at Virginia Polytechnic Institute and State University.
During his visiting NAU, he will give the following lectures:

10/1 a.m. 8:30-10:30: Lecture 1. Genome sequencing technolgies, including sequence assembly and next generation technologies；
10/1 p.m. 2:30-4:30: Lecture 2. Gene prediction and structural annotation in genome sequences；
10/2 a.m. 8:30-10:30: Lecture 3. Functional prediction of genes in genome sequences；
10/2 p.m. 2:30-4:30: Lecture 4. Functional genomics: transcriptional profiling；
10/3 a.m. 8:30-10:30: Lecture 5. Resources for oomycete genomics；
10/4 a.m. 8:30-10:30: Lecture 6. Research seminar: "Structural and Functional Genomics of Oomycete
pathogens."
10/5 a.m. 8:30-10:30: Lecture 7. Oomycetes avirulence genes, effectors and the RXLR-dEER motif

group seminar in English from now on

Last week our microRNA group seminar tried in English. To our boss's expectation, we had a very good show in discussion. 'So, let's have seminar in Enlish from now on! ' we are encouraged to speak English and express oneself freely. Oh, my god! It's my turn next seminar!

Science and Lab Jokes

The Fox and Rabbit - a Graduate Student Tale
In a forest a fox bumps into a little rabbit, and says, "Hi, junior, whatare you up to?""I'm writing a dissertation on how rabbits eat foxes," said the rabbit."Come now, friend rabbit, you know that's impossible!""Well, follow me and I'll show you."They both go into the rabbit's dwelling and after a while the rabbit emergeswith a satisfied expression on his face.
Along comes a wolf. "Hello, what are we doing these days?""I'm writing the second chapter of my thesis, on how rabbits devour wolves.""Are you crazy? Where is your academic honesty?""Come with me and I'll show you." ......As before, the rabbit comes out with a satisfied look on his faceand this time he has a diploma in his paw.The camera pans back and into the rabbit's cave and, as everybody shouldhave guessed by now, we see an enourmous mean-looking lion sitting nextto the bloody and furry remains of the wolf and the fox.The moral of this story is:It's not the contents of your thesis that are important --it's your PhD advisor that counts.

Scientist: Four golden lessons

Nature 426, 389 (27 November 2003); doi:10.1038/426389a　
Scientist: Four golden lessons 　　
STEVEN WEINBERG
Steven Weinberg is in the Department of Physics, the University of Texas at Austin, Texas 78712, USA. This essay is based on a commencement talk given by the author at the Science Convocation at McGill University in June 2003.　　　　　　

When I received my undergraduate degree — about a hundred years ago — the physics literature seemed to me a vast, unexplored ocean, every part of which I had to chart before beginning any research of my own. How could I do anything without knowing everything that had already been done? Fortunately, in my first year of graduate school, I had the good luck to fall into the hands of senior physicists who insisted, over my anxious objections, that I must start doing research, and pick up what I needed to know as I went along. It was sink or swim. To my surprise, I found that this works. I managed to get a quick PhD — though when I got it I knew almost nothing about physics. But I did learn one big thing: that no one knows everything, and you don‘t have to.　　　　

Another lesson to be learned, to continue using my oceanographic metaphor, is that while you are swimming and not sinking you should aim for rough water. When I was teaching at the Massachusetts Institute of Technology in the late 1960s, a student told me that he wanted to go into general relativity rather than the area I was working on, elementary particle physics, because the principles of the former were well known, while the latter seemed like a mess to him. It struck me that he had just given a perfectly good reason for doing the opposite. Particle physics was an area where creative work could still be done. It really was a mess in the 1960s, but since that time the work of many theoretical and experimental physicists has been able to sort it out, and put everything (well, almost everything) together in a beautiful theory known as the standard model. My advice is to go for the messes — that‘s where the action is.　

My third piece of advice is probably the hardest to take. It is to forgive yourself for wasting time. Students are only asked to solve problems that their professors (unless unusually cruel) know to be solvable. In addition, it doesn‘t matter if the problems are scientifically important — they have to be solved to pass the course. But in the real world, it‘s very hard to know which problems are important, and you never know whether at a given moment in history a problem is solvable. At the beginning of the twentieth century, several leading physicists, including Lorentz and Abraham, were trying to work out a theory of the electron. This was partly in order to understand why all attempts to detect effects of Earth‘s motion through the ether had failed. We now know that they were working on the wrong problem. At that time, no one could have developed a successful theory of the electron, because quantum mechanics had not yet been discovered. It took the genius of Albert Einstein in 1905 to realize that the right problem on which to work was the effect of motion on measurements of space and time. This led him to the special theory of relativity. As you will never be sure which are the right problems to work on, most of the time that you spend in the laboratory or at your desk will be wasted. If you want to be creative, then you will have to get used to spending most of your time not being creative, to being becalmed on the ocean of scientific knowledge.　　
　　
Finally, learn something about the history of science, or at a minimum the history of your own branch of science. The least important reason for this is that the history may actually be of some use to you in your own scientific work. For instance, now and then scientists are hampered by believing one of the over-simplified models of science that have been proposed by philosophers from Francis Bacon to Thomas Kuhn and Karl Popper. The best antidote to the philosophy of science is a knowledge of the history of science.　　　　

More importantly, the history of science can make your work seem more worthwhile to you. As a scientist, you‘re probably not going to get rich. Your friends and relatives probably won‘t understand what you‘re doing. And if you work in a field like elementary particle physics, you won‘t even have the satisfaction of doing something that is immediately useful. But you can get great satisfaction by recognizing that your work in science is a part of history.　
　　　
Look back 100 years, to 1903. How important is it now who was Prime Minister of Great Britain in 1903, or President of the United States? What stands out as really important is that at McGill University, Ernest Rutherford and Frederick Soddy were working out the nature of radioactivity. This work (of course!) had practical applications, but much more important were its cultural implications. The understanding of radioactivity allowed physicists to explain how the Sun and Earth‘s cores could still be hot after millions of years. In this way, it removed the last scientific objection to what many geologists and paleontologists thought was the great age of the Earth and the Sun. After this, Christians and Jews either had to give up belief in the literal truth of the Bible or resign themselves to intellectual irrelevance. This was just one step in a sequence of steps from Galileo through Newton and Darwin to the present that, time after time, has weakened the hold of religious dogmatism. Reading any newspaper nowadays is enough to show you that this work is not yet complete. But it is civilizing work, of which scientists are able to feel proud.

科学家：四条黄金忠告 【梳枝/译】

Steven Weinberg　　　　

Steven Weinberg 现在得克萨斯大学物理系。本文以他 2003年6月在麦克基尔大学科学大会上的讲话为基础。　　　　　　

当我得到大学学位的时候 － 那是百八十年前的事了 －物理文献在我眼里就象一个未经探索的汪洋大海，我必须在勘测了它的每一个部分之后才能开始自己的研究。做任何事情之前怎么能不先了解所有已经做过了的工 作呢？万幸的是，在我做研究生的第一年，我碰到了一些资深的物理学家，他们不顾我忧心忡忡的反对坚持我应该开始进行研究，而在研究的过程中学习所需的东 西。这可是生死悠关的事。我惊讶地发现他们的意见是可行的。我设法很快就拿到了一个博士学位 －虽然我拿到博士学位时对物理学还几乎是一无所知。不过，我的确得到了一个很大的教益：没有人了解所有的知识，你也不必。　
　　　
另一个忠告就是，如果继续用我的海洋学的比喻的话，当你在大海中搏击而不是沉没时，应该到波涛汹涌的地方去。20世纪60年代末，我在麻省理工大学教书 时，一个学生找我说，他想去做广义相对论领域的研究，而不愿意做我所在的领域－基本粒子物理学－方向的研究，原因是前者的原理已经很清楚，而后者在他看来 则是一团乱麻。而在我看来这正是做相反决定的绝好理由。粒子物理学是一个还可以做创造性工作的领域。它在那个时候的确是乱麻一团，但是，从那时起，许多理 论物理学家、试验物理学家的工作把这团乱麻梳理出来，将所有的（嗯，几乎所有的）知识纳入一个叫做标准模型的美丽的理论之中。我的忠告是：到混乱的地方 去，那里才是行动所在的地方。　　　　

我的第三个忠告可能是最难被接受的。这就是要原谅自己虚掷时光。要求学生们解决的问题都是教授们知道可以得到解决的问题（除非教授非常地残酷）。而 且，这些问题在科学上是否重要是无关紧要的，－必须解决他们以通过考试。但是在现实生活中，知道哪些问题重要是非常困难的，而且在历史某一特定时刻你根本 无从知道某个问题是否有解。二十世纪初，几个重要的物理学家，包括 Lorentz 和 Abraham, 想创立一种电子理论。部分原因是为了理解为什么探测地球相对以太运动的所有尝试都失败了。我们现在知道，他们研究的问题不对。在当时，没有人能够创立一个 成功的电子理论，因为量子力学尚未发现。需要到1905年，天才的爱因斯坦认识到正确的问题是运动在时间空间测量上的效应。沿着这条路线，他创立了相对 论。因为你总也不能肯定哪个才是要研究的正确问题，你在实验室里，在书桌前的大部分时间是会虚掷的。如果你想要有创制性，你就必须习惯于大量时间不是创造 性的，习惯于在科学知识的海洋上停滞不前。　

最后，学一点科学史，起码你所研究的学科的历史。至少学习科学史可能在你自己的科学研究中有点用。比如，科学家会不时因相信从培根到库恩、玻普这些哲学家所提出的过分简化的科学模型而受到桎梏。科学史的知识是科学哲学的最好解毒剂。　
　　　
更重要的是，科学史的知识可以使你觉得自己的工作更有意义。作为一个科学家，你很可能不会太富裕，你的朋友和亲人可能也不理解你正在做的事情。而如果你研 究的是象基本粒子物理学这样的领域，你甚至没有是在从事一种马上就有用的工作所带来的满足。但是，认识到你进行的科学工作是历史的一部分则可以给你带来极 大的满足。　　　　

看看100年前，1903年。谁是1903年大英帝国的首相、谁是1903年美利坚合众国的总统在现在看来有多重要呢？真正凸现出重要性的是 1903年Ernest Rutherford 和Frederick Soddy 在McGill 大学揭示了放射性的本质。这一工作（当然！）有实际的应用，但更加重要的是其文化含义。对放射性的理解使物理学家能够解释为什么几百万年以后太阳和地心仍 是滚烫的。这样，就清除了许多地质学家和古生物学家认为地球和太阳存在了很长年代的最后一个科学上的障碍。从此以后，基督教徒和犹太教徒就不得不或者放弃 圣经的直接真理性或者把它当成与理智无关的东西。这只是从加利略到牛顿、达尔文，直到现在削弱宗教教条主义桎梏的一系列步伐中的一步。只要读读今天的任何 一张报纸，你都会知道这一工作还没有完成。但是，这是一个文明化的工作，对这一工作科学家是可以感到骄傲的。

Turn proteins into music

When I'm listening to the sound of a protein, I can't help speaking out: wonderful! Look, scientific jobs are not boring and can be injected with art particles!
Contributors: A classically-trained pianist and microbiologist at the University of California at San Diego, who has been "musicalising" the proteins along with colleague, Jeffrey Miller.
Article: Rie Takahashi and Jeffrey H Miller, Conversion of amino-acid sequence in proteins to classical music: search for auditory patterns, Genome Biology (In press)
Further examples of converted proteins and the computer program are accessible for online use [www.mimg.ucla.edu/faculty/miller_jh/gene2music/home.html]. The browser allows anyone to send in a sequence coding for a protein that is then converted into music.

Excellence is a habit

my boss told his students us today:
“We are what we repeatedly do. Excellence, then, is not an act, but a habit. ---Aristotle”>“我们每一个人都是由自己一再重复的行为所铸造的。因而优秀不是一种行为，而是一种习惯。---亚里士多德”

Parkinson's Disease: Nicotine Could Help; Pesticides Harm

Science Daily — The Parkinson's Institute recently announced new findings concerning the role of environmental factors in the development of Parkinson's disease.
Highlights of the research include:
The role of pesticides (eg. Paraquat and Dieldrin) as potential risk factors for Parkinson's disease, a role suggested by both epidemiological statistics and laboratory evidence.
The threat of toxic agents to damage neurons by causing the accumulation of harmful proteins.
Intraneuronal protein aggregates as markers of Parkinson's pathology, based on work carried out at The Parkinson's Institute indicating that these aggregates could be formed as a consequence of toxic exposure.
The importance of targeting a specific protein, alpha-synuclein, in order to achieve neuroprotection in Parkinson's
The role of inflammation in the development of Parkinson's disease and the possibility that anti-inflammatory drugs could be beneficial to patients.
The possibility that nicotine may act as a neuroprotective agent.
These results will be reported at Asilomar (Pacific Grove, CA) as part of the final meeting of the Collaborative Centers for Parkinson's Disease Environmental Research (CCPDER). This collaborative research effort, sponsored by the National Institute of Environmental Health Sciences (NIEHS), brings together investigators from Emory University, the University of California Los Angeles and The Parkinson's Institute, which has served as the coordinating center for the study.
"Our collaboration with Emory University and UCLA has allowed us to make great strives in identifying environmental factors involved in the development of Parkinson's disease," said Donato A. Di Monte, M.D., director of basic research at The Parkinson's Institute. "The findings that will be discussed at Asilomar will help us better understand the disease process, intervene earlier with neuroprotective treatment and work on preventive measures against Parkinson's disease risk factors."
Note: This story has been adapted from a news release issued by The Parkinson's Institute.
Source:
The Parkinson's Institute
Date:
April 5, 2007

April Fools' day

The day before yesterday, I noted that gmail introduce a new service for gmail users——gmail paper , how funny! I couldn't image what we can get from google across the pacific ocean! Then I realized that I was fooled by google, because i couldn't find the next linker to get the sigh up for gmail paper! :)

Social Life Of Honeybees Coordinated By A Single Gene

Science Daily — Students of the evolution of social behavior got a big boost with the publication of the newly sequenced honeybee genome in October 2006. The honeybee (Apis mellifera) belongs to the rarified cadre of insects that pool resources, divide tasks, and communicate with each other in highly structured colonies. Understanding how this advanced state of organization evolved from a solitary lifestyle has been an enduring question in biology.

A honeybee gene originally used in egg production has become an important behavioral modulator and a timekeeper of social life. (Credit: Siri-Christine Seehuus / PLoS Biology)
In a new study published in PLoS Biology, Mindy Nelson, Kate Ihle, Gro Amdam, and colleagues reveal one possible path to community by showing that a single gene controls multiple traits related to honeybee sociability. First characterized for its role in reproduction, the gene, vitellogenin, is widely found in egg-laying insects, which depend on it for egg cell development.

A honeybee's lot in life depends on its age, gender, and caste. Reproduction falls to the queen and drones, while essentially infertile females, the workers, perform all the other duties required to support the colony. As young adults, workers tend larvae and perform assorted tasks in the hive. After about three weeks, they switch from domestic chores to foraging, and eventually specialize in pollen or nectar collection.

Scientists began to suspect that the protein synthesized from the vitellogenin gene--vitellogenin--might affect these social life history traits in honeybees as it became clear that the protein supported an array of functions not directly linked to egg-laying. For example, sterile workers synthesize vitellogenin to make the royal jelly they feed larvae. It can also prolong the lifespan of both workers and the queen by reducing oxidative stress.

As bees undergo the complex behavioral shift demanded by the change in job description, their physiology changes too: they have higher levels of juvenile hormone and lower levels of vitellogenin. It was speculated that these two physiological factors repress each other to affect the bees' behavior, with vitellogenin repressing juvenile hormone in younger bees to inhibit the shift from nest to field, and juvenile hormone repressing vitellogenin in bees that have switched to foraging to ensure that they stay true to their task and do not revert to nest jobs. In a previous study, the researchers also proposed that changes in vitellogenin gene expression early in life could foster the selective behavior that creates the division of labor between pollen and nectar specialists.

To test these proposed roles of vitellogenin in coordinating the social life of the honeybee, Nelson et al. inhibited the expression of the vitellogenin gene with RNA interference (RNAi). This gene-silencing tool introduces a double-stranded RNA (dsRNA) product whose sequence is complementary to a target gene, thereby setting off a series of events that ultimately "knocks down" the target gene. The researchers injected a vitellogenin dsRNA preparation into the abdomen of a subset of bees and compared their behavior and lifespan to a control group. (The control group also received a dsRNA treatment designed to mimic the stress of experimental handling without affecting gene expression.) The bees' vitellogenin levels were monitored at 10 days, 15 days, and 20 days old to make sure the RNAi effects persisted.

Compared to controls, dsRNA-treated bees had consistently lower levels of vitellogenin protein. These vitellogenin "knockdowns" started foraging at a younger age than controls--confirming that vitellogenin affects workers' occupational fate by repressing the shift from domestic to foraging tasks. The foragers also showed a preference for nectar, in keeping with evidence that workers genetically predisposed toward nectar have lower vitellogenin levels before leaving the nest, while those predisposed toward pollen have higher levels. But more directly, the researchers argue, these results show that vitellogenin controls social foraging specialization. What's more, the vitellogenin-deficient bees died earlier than the controls, demonstrating the protein's influence on honeybee longevity.

Altogether, these results demonstrate that vitellogenin regulates the organizational structure of honeybee society by influencing workers' division of labor and foraging preference. Vitellogenin, the researchers conclude, controls not only when bees start foraging and how long they live, but what they forage. Higher levels early in life favor pollen; lower levels favor nectar. Since current methods cannot yet distinguish the effects of vitellogenin from those of juvenile hormone, the researchers argue that the two physiological factors should be considered as partners in mediating task assignment and specialization. Since this partnership is uncommon in insects, it suggests that social behavior in honeybees emerged from a makeover of relations between vitellogenin and juvenile hormone. It also bolsters the notion that factors normally in control of female reproduction can lay the foundation for the transition from solitary life to complex social behavior.

Citation: Nelson CM, Ihle KE, Fondrk MK, Page RE Jr, Amdam GV (2007) The gene vitellogenin has multiple coordinating effects on social organization. PLoS Biol 5(3): e62. doi:10.1371/journal.pbio.0050062.
Source: Public Library of Science Date: March 18, 2007

Fruit Flies May Pave Way To New Treatments For Age-related Heart Disease

Science Daily — The tiny Drosophila fruit fly may pave the way to new methods for studying and finding treatments for heart disease, the leading cause of death in industrialized countries, according to a collaborative study by the Burnham Institute for Medical Research, UC San Diego (UCSD) and the University of Michigan.
The study reports that mutations in a molecular channel found in heart muscle cell membranes caused arrhythmias similar to those that are found in humans, suggesting that understanding how this channel's activity is controlled in the cell could lead to new heart disease treatments. Led by Burnham's Professor Rolf Bodmer, Ph.D., and Staff Scientist Karen Ocorr, Ph.D., these new results,are to be published in Proceedings of the National Academy of Sciences.
"This study shows that the Drosophila heart can be a model for the human heart," said Burnham researcher Bodmer. "Fly hearts have many ion channels that also are present in human hearts, making it suitable to extend mechanistic insight found in the fly hearts to human heart function."
The researchers focused on a membrane channel in the tiny Drosophila heart called KCNQ. This membrane channel, found in flies and humans, regulates the heart's ability to return to a relaxed state after beating. This ability is crucial to healthy cardiac functions, and the inability to return to a relaxed state results in arrhythmias, which can lead to more serious heart disease and sudden death. In both flies and humans, cardiac arrhythmia and dysfunctions become more common with age.
The team found that mutations in the fly's single KCNQ gene led to severe arrhythmias that would be immediately fatal to a human, but not in this insect that does not rely on the heart for oxygen supply. Hearts in young flies with the KCNQ mutation exhibited prolonged heart contractions and irregular beats seen usually in older flies (and older people). To enable their study of the fly heart, the researchers created new methods to dissect the hearts, and quantify heart contractility and other functions by using a movie camera to capture fly's cardiac activity.
"We started with Nick Reeves and James Posakony at UCSD, who originally made the mutant KCNQ fly for a different purpose. We then studied these mutants with the new heart function assays that Ocorr was developing in my lab. Subsequently, we worked with Martin Fink and Wayne Giles at UCSD to develop a computer program that would allow the automated quantification of heart beat parameters and arrhythmias from the video images," Bodmer said. In addition, collaborations with H.S. Vincent Chen at Burnham and Soichiro Yasuda and Joseph Metzger of the University of Michigan enabled measuring the fly's electrocardiogram (ECG) and heartbeat force and tension, respectively.
"We now have a lot of methods to precisely assess heart function in the fly, which augments its usefulness as a genetic model for studying cardiac function," said Ocorr, who conducted most of these studies.
The study points to KCNQ as a major factor in heart disease, but Bodmer warns that much more research is needed to use it alone as a drug target. "The fact that heart functions deteriorate in the mutant flies during aging suggests that there are other channels and genes that contribute to cardiac aging," he said. "We need to better understand the regulatory systems that control the level and activity of known cardiac channels and other unknown factors involved in coordinated heart muscle contraction."
In fact, the researchers are now looking at identifying other genes that regulate KCNQ channel function and heart physiology, and--thanks to the short lifespan of Drosophila --can look at the effects of aging, which is much harder to do in mammals with a relatively long lifespan.
"There's an amazing conservation of genes between flies and humans," Bodmer said. "We can now look at how heart function ages in a realistic timeframe."
In addition to first author Ocorr, and contributions from collaborators Reeves, Fink, Chen, Yasuda, Posakony, Giles and Metzger, Bodmer's colleagues included Robert Wessells and Takeshi Akasaka at Burnham.
"The collaborative spirit at Burnham", said Bodmer, "greatly facilitated interactions among the researchers that brought this multidisciplinary study to fruition".
This work was supported by grants from the National Institutes of Health, as well as private support to H.S. Vincent Chen at Burnham from the American College of Cardiology Foundation.
Note: This story has been adapted from a news release issued by Burnham Institute.
Source:Burnham InstituteDate:March 12, 2007

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Fruit Fly Insight Could Lead To New Vaccines

Science Daily — The tiny fruit fly has a lot to teach humans. Researchers at the Stanford University School of Medicine have found for the first time that flies' primitive immune systems may develop long-term protection from infection, an ability previously thought impossible for insects.
The findings could have implications for new ways of developing human vaccines, especially for people with compromised immune systems.
The evidence that a fruit fly's immune response can adapt to - or retain memory of - an earlier infection contradicts the long-held dogma that immune memory cannot exist in invertebrates such as insects. Such memory of a specific pathogen, known as adaptation, is supposed to be a hallmark of the higher-level immune system response of humans and other vertebrates.
The Stanford work raises the possibility that humans could make use of this rudimentary immune response if their higher-level system is crippled. "It's a springboard to looking at the immune system in a whole new way," said David Schneider, PhD, assistant professor of microbiology and immunology and senior author of the study, which will be published in the Public Library of Science-Pathogens.
One of the two arms of the immune response in higher organisms is similar to that of flies. This arm is known as innate immunity, and it is thought to be a primitive first-line, nonspecific response to a pathogen "invader." The other arm found in higher organisms is adaptive immunity, which has a memory that retains an internal record of contact with an invader and - employing T and B cells - springs into action once it encounters the same invader again. This adaptive immunity explains why a vaccine provides protection.
"AIDS patients are like fruit flies in the sense that they don't have properly functioning T cells," said Schneider. "If there is anything we could do to make their remaining innate immunity better through adaptation, that would be really helpful."
Harnessing the potential power of adaptation in the innate immune system might also be a boon in the body's defense against bioterrorism or disease pandemics. "The B and T cells of the adaptive immune system take a long time to react," said Schneider. "But you might be able to speed things up if you could snort something up your nose that would make your innate immune system ready to fight."
While inviting novel ways of thinking about future vaccines and treating AIDS patients, the new finding immediately stirs up the field of insect immunology. Existing publications about the fruit fly's immune system explicitly state that it has no memory, and no ability to make specific long-term changes prompted by its exposure to pathogens. Because immune memory was defined as nonexistent, no one ever did the experiment to question whether the fly's immune system could adapt.
Then graduate student Linh Pham arrived in Schneider's lab. She was interested in pushing the boundaries of the assumptions of the innate immune system's limitations.
In the past decade or so, work done on fruit fly immunology has always been done on a fly infected only once - and that's not how things happen outside a lab, where a fly would be continually exposed to microbes. Pham thought to ask what happens when the flies encounter a microbe a second time.
Pham found a bacterium - Streptococcus pneumoniae - that infected the flies but didn't kill all of them. "I liken my work to the first vaccination experiments," said Pham, who is first author of the study. She essentially vaccinated over a million flies, typically doing 7,000 in a day, in numerous experiments. In a key experiment, she injected some flies with killed bacteria and others with just saline solution. She waited a week, then reinjected both groups with what should have been a lethal dose of live bacteria. Then she calculated the percentage of how many survived, compared with the flies that been injected only with saline.
"I didn't think the results would be so clean-cut," she said. Within two days, the second dose killed almost all of the flies that had initially received just saline solution. Those that had been vaccinated lived just as long - about one month - as a separate group that had not been infected.
To ensure it wasn't a fluke of the bacterium she chose, she tested other organisms. She identified a fungus that infects fruit flies in the wild, Beauveria bassiana, that elicited a similar protective effect. "It was really easy to show the adaptation part," she added. "Getting to the mechanism was the complicated part."
In the study, the researchers conclude that a much-studied receptor called Toll is involved, as are other processes. Pham is now teasing apart the finer aspects of how the fruit fly protects itself against S. pneumoniae.
Schneider and Pham said they hope their work encourages the search for a similar adaptive response in the innate immune systems of humans or other vertebrates. "One of the things that I thought was really cool about this work is that it might be a way to develop a vaccine that modulates the innate immune system," said Pham. "Of course, we are cautious about hoping for this."
Note: This story has been adapted from a news release issued by Stanford University Medical Center.
Source:Stanford University Medical Center Date:March 11, 2007

Holographic Images look into Biology

Holographic Images Use Shimmer To Show Cellular Response To Anticancer Drug
Science Daily — The response of tumors to anticancer drugs has been observed in real-time 3-D images using technology developed at Purdue University. The new digital holographic imaging system uses a laser and a charged couple device, or CCD, the same microchip used in household digital cameras, to see inside tumor cells. The device also may have applications in drug development and medical imaging.
"This is the first time holography has been used to study the effects of a drug on living tissue," said David D. Nolte, the Purdue professor of physics who leads the team. "We have moved beyond achieving a 3-D image to using that image for a direct physiological measure of what the drug is doing inside cancer cells. This provides valuable information about the effects of various doses of the drug and the time it takes each dose to become significantly effective."
The laser is gentle and does not harm living tissue, Nolte said. The cancer cells used for the research were grown independently in a bioreactor in the laboratory.
Holography uses the full spectrum of information available from light, more than what the human eye can detect, to create a 3-D image called a hologram. By shining a laser on both the object and directly on the CCD chip of the digital camera, the system screens the pattern of light reflected back from the object and allows the camera to record very detailed information, including depth and motion on a scale of microns, or 0.0001 centimeter.
The scattered light waves reflected back from the object come together at the camera's detector and form what is called "laser speckle." To the eye, this speckle appears as a random pattern of blotches of bright and dark, but the pattern changes if there is motion within the object.
"All living matter is in constant motion, and the laser speckle from a living object is constantly changing with that motion," Nolte said. "This was the key to the diagnostic ability of the technique. The image appears to shimmer with the motion inside the cell. As the anticancer drug works, there is less motion inside the cell and the shimmer effect is reduced. This can be seen right on the screen."
The findings of this National Science Foundation funded research was detailed in an oral presentation on Tuesday (March 6) at the American Physical Society Meeting in Denver, Colo. The team was selected from more than 7,000 submissions as one of 25 to present results at a meeting press conference. John Turek, a professor of basic medical sciences at Purdue, and Kwan Jeong, a graduate assistant, collaborated with Nolte on this work.
The team detects the motion of organelles inside cancer cells. Organelles are tiny specialized structures that perform internal cell functions and are a common target of anticancer drugs because they play a key role in the uncontrolled cell division that makes cancer lethal.
Colchicine, the anticancer drug studied by the group, limits the ability of organelles to travel throughout the cell and perform their functions. The drug disrupts the growth of microtubules, the highways of the internal cellular structure, and leaves organelles stuck at dead ends unable to move.
This reduction in motion translates to less shimmer in the image on the screen and can be quantitatively analyzed by a computer program, Nolte said.
"Let's say there are 1,000 organelles reflecting light; the exact pattern of the laser speckle is sensitive to each organelle's location," he said. "If one moves even one-half micron, then the pattern changes. It is highly dynamic and sensitive to changes."
In addition to the technology's sensitivity to motion, the field of view is unique because of its "dynamic range," the difference between the largest and smallest scale accessed.
"We can look at a fairly large section of the object, about a 30-micron-thick section of a 700-micron-thick tumor," Nolte said. "At the same time, we can retrieve information within the micron scale.
"Biologists currently have to look at things on the cellular level through microscopes. With this technology, we now can detect things on the cellular level and the tissue scale at the same time. In this case, the whole is greater than the sum of its parts. Tissue is more than just an accumulation of cells. It is a communication network in 3-D that behaves differently than 2-D cell cultures."
In addition to realizing the diagnostic applications of the shimmer, the group has simplified and reduced the cost of the system.
In 2002 Nolte's group was the first to use holography to produce images inside of tissue. The original technique used special semiconductor holographic film developed by the team as opposed to a CCD chip.
"At the time, the only way to capture the image was on this very expensive, very difficult to make film," Nolte said. "But the CCD cameras kept getting better and better and reached the point where we could make the transition from holographic film to the CCD."
Light waves have peaks and valleys that offer information about depth undetected by the human eye. By shining a second laser directly on the CCD chip, bright and dark fringes occur corresponding to the relationship of these peaks and valleys. These fringes, or interference patterns, can be recorded directly onto the camera.
"This extra laser light wave, called the reference wave, acts like a yardstick," Nolte said. "It provides depth information and measurement. It gives us the original image layered with the fringes and the specific locations of these fringes tell us about the 3-D structure of the object."
The team combines this holography technique with "laser ranging," a method similar to radar that measures the time it takes for a laser pulse to travel to an object and be reflected back.
"The holography gives us the peaks and valleys and detailed depth information, while the laser ranging allows us to control how deep we are looking," he said.
The team plans to make measurements of the cytoskeleton, the support structure of cells, and to further examine what types of motion influence the shimmer effect.
"What we have seen is just the tip of the iceberg," Nolte said.
Note: This story has been adapted from a news release issued by Purdue University. Source:Purdue UniversityDate:March 9, 2007

Seminar

This afternoon on group's regular seminar, I was triggered by our boss to explain a conception. I know of it fully, so stand up, walk straightforwardly to the white board to address, but failed. Everybody even seemed more confused after my expression. At last one of my senior classmate helped me. Then i asked myself, too nervous? No! Maybe I didn't open my mouth appropriately, express my brain right, maybe i should practise more to improve my oral skill. :)
In addition, we should bear in mind that IDEA and CREATIVITY is the origin and spirit of Science.

Next-generation sequencing outpaces expectations

News
Nature Biotechnology - 25, 149 (2007) Published online: 1 February 2007; doi:10.1038/nbt0207-149
Catherine Shaffer
Ann Arbor, Michigan
Growing demand in both the research and clinical markets is fueling the development – and funding – of more efficient genomic sequencing methods.
"The market for next generation sequencing technology already stands at $1 billion driven largely by resequencing efforts." John Sullivan Leerink SwanBoston

On January 8, Solexa, of Hayward, California, announced the completion of an early-access program evaluating its next-generation Genome Analysis system with customers and reiterated its intention to begin full commercial sales this quarter. Two months earlier, in anticipation of the entry of Solexa's technology and wanting a piece of the emerging market for whole-genome resequencing and analysis, San Diego, California–based microarray maker Illumina announced its intention to acquire the firm in a stock-for-stock transaction valued at around $600 million (Nat. Biotechnol. 25, 10, 2007).On the completion of the merger, the new Solexa-Illumina business combination will join several other companies currently pushing the boundaries of sequencing technology. Curagen spin-off 454 Life Sciences, of Branford, Connecticut, and Agencourt Personal Genomics in Beverly, Massachusetts, a part of Applied Biosystems Group, are already on the market with systems that bring sequencing costs down several orders of magnitude below the millions of dollars per genome cost associated with capillary-array electrophoresis (CAE) sequencing—the technology that made possible the Human Genome Project a mere six years ago. Cambridge, Massachusetts–based Helicos Biosciences, for its part, claims that its single-molecule sequencing technology, expected to debut in the second half of the year, will enable the sought-after '$1,000 genome' price point, although not immediately. Smaller companies are also merging their respective technologies in an attempt to stay competitive in this technology race.The intense activity in part stems from a pent-up and growing demand in both the research and clinical markets—the dynamic that Illumina identified in its discussions with customers, leading to the bid for Solexa. Indeed, the field appears to be advancing more rapidly than originally envisioned. According to John Sullivan, equity research analyst at Leerink Swann in Boston, the market for next-generation sequencing technology already stands at $1 billion, driven largely by targeted resequencing efforts aimed at finding genetic variations and rare mutations that contribute to complex diseases.
In 2004, the National Human Genome Research Institute (NHGRI) proposed a way to achieve affordable human genome sequencing by 2014, in two increments. NHGRI program director Jeff Schloss explains: "The way the [Requests for Applications] were laid out, at the time we launched the program, we were hoping the $100,000 genome might come in five years. The goal for $1,000 was to be five years after that." Solexa has already sequenced a gigabase at the $100,000 cost benchmark, making it the first company to announce the achievement of the first goal.
NHGRI wants the advantage of next-generation sequencing tools for its comparative genomics projects. The Cancer Genome Project, under the auspices of the National Institutes of Health, also suggests a nearly bottomless market for affordable gene sequencing. More speculatively, an affordable genome could make the dream of personalized medicine a reality, by enabling the sequencing of an individual's genome at a cost low enough to allow the information to become a routine part of one's medical record.
One of the newest winners of NHGRI's $100,000 genome grant, Intelligent Bio-Systems, of Waltham, Massachusetts, is developing a four-color sequencing-by-synthesis method using cleavable fluorescent nucleotide reversible terminators—an approach similar to that of Solexa. It is placing instruments in selected laboratories for beta testing, with a technology that features faster run cycles, less up-front expense and less costly implementation. "We're trying to design the system so that when the market is ready, it could actually be placed into a clinical laboratory," says CEO Steven Gordon. "The instrument cost is low enough that it could be used for clinical tests."
Companies have also started to win bids under the NHGRI $1,000 genome program. Unlike the $100,000 technologies, which focus on refining and improving existing methods, the conception of a $1,000 genome requires an entirely different paradigm—a discontinuous innovation. Helicos' technology, unlike the cluster-based approaches of 454, Agencourt and Solexa, could provide such a leap: in the first commercial award under the $1,000 program, it received, in October 2006, a $2 million grant to further develop its single-molecule approach.
According to Steve Lombardi, senior vice president of Marketing at Helicos, "If you had perfect chemistry, and each step was 99.99%, the instrument would generate 100 billion bases a day. The instrument is being designed for that throughput, but the first-generation chemistry will have a smaller yield—around 600 megabases per day." Improvements in chemistry could move Helicos to the $1,000 genome "in the first few years," he claims—well ahead of the NHGRI goal of 2014.
Over its three-year history, Helicos has raised $67 million in venture funding; the figure for Solexa was well over $100 million. Venture capitalists' appetite for these technologies is still strong. In December 2006, Pacific Biosciences of Menlo Park, California, raised $50 million in venture capital to further develop its single-molecule detection system, first published in 2003 (Science 299, 682–686, 2003). Others are combining forces to gain the resources and technology breadth to compete. Also in December, NABsys, Inc. of Providence, Rhode Island, which has a $1,000 genome technology with a three-year delivery goal, according to CEO Barret Bready, acquired GeneSpectrum, merging its nanopore technology with GeneSpectrum's DNA hybridization technology to create hybridization-assisted nanopore sequencing.
Published online: 1 February 2007.

What is junk DNA, and what is it worth

from Science American ASK THE EXPERTS: BIOLOGY
What is junk DNA, and what is it worth?
A. Khajavinia

Wojciech Makalowski, a Pennsylvania State University biology professor and researcher in computational evolutionary genomics, answers this query.
Our genetic blueprint consists of 3.42 billion nucleotides packaged in 23 pairs of linear chromosomes. Most mammalian genomes are of comparable size—the mouse script is 3.45 billion nucleotides, the rat's is 2.90 billion, the cow's is 3.65 billion—and code for a similar number of genes: about 35,000. Of course, extremes exist: the bent-winged bat (Miniopterus schreibersi) has a relatively small 1.69-billion-nucleotide genome; the red viscacha rat (Tympanoctomys barrerae) has a genome that is 8.21 billion nucleotides long. Among vertebrates, the highest variability in genome size exists in fish: the green puffer fish (Chelonodon fluviatilis) genome contains only 0.34 billion nucleotides, while the marbled lungfish (Protopterus aethiopicus) genome is gigantic, with almost 130 billion. Interestingly, all animals have a large excess of DNA that does not code for the proteins used to build bodies and catalyze chemical reactions within cells. In humans, for example, only about 2 percent of DNA actually codes for proteins.
For decades, scientists were puzzled by this phenomenon. With no obvious function, the noncoding portion of a genome was declared useless or sometimes called "selfish DNA," existing only for itself without contributing to an organism's fitness. In 1972 the late geneticist Susumu Ohno coined the term "junk DNA" to describe all noncoding sections of a genome, most of which consist of repeated segments scattered randomly throughout the genome.
Typically these sections of junk DNA come about through transposition, or movement of sections of DNA to different positions in the genome. As a result, most of these regions contain multiple copies of transposons, which are sequences that literally copy or cut themselves out of one part of the genome and reinsert themselves somewhere else.
Elements that use copying mechanisms to move around the genome increase the amount of genetic material. In the case of "cut and paste" elements, the process is slower and more complicated, and involves DNA repair machinery. Nevertheless, if transposon activity happens in cells that give rise to either eggs or sperm, these genes have a good chance of integrating into a population and increasing the size of the host genome.
Although very catchy, the term "junk DNA" repelled mainstream researchers from studying noncoding genetic material for many years. After all, who would like to dig through genomic garbage? Thankfully, though, there are some clochards who, at the risk of being ridiculed, explore unpopular territories. And it is because of them that in the early 1990s, the view of junk DNA, especially repetitive elements, began to change. In fact, more and more biologists now regard repetitive elements as genomic treasures. It appears that these transposable elements are not useless DNA. Instead, they interact with the surrounding genomic environment and increase the ability of the organism to evolve by serving as hot spots for genetic recombination and by providing new and important signals for regulating gene expression.
Genomes are dynamic entities: new functional elements appear and old ones become extinct. And so, junk DNA can evolve into functional DNA. The late evolutionary biologist Stephen Jay Gould and paleontologist Elisabeth Vrba, now at Yale University, employed the term "exaptation" to explain how different genomic entities may take on new roles regardless of their original function—even if they originally served no purpose at all. With the wealth of genomic sequence information at our disposal, we are slowly uncovering the importance of non-protein-coding DNA.
In fact, new genomic elements are being discovered even in the human genome, five years after the deciphering of the full sequence. Last summer developmental biologist Gill Bejerano, then a postdoctoral fellow at the University of California, Santa Cruz, and now a professor at Stanford University, and his colleagues discovered that during vertebrate evolution, a novel retroposon—a DNA fragment, reverse-transcribed from RNA, that can insert itself anywhere in the genome—was exapted as an enhancer, a signal that increases a gene's transcription. On the other hand, anonymous sequences that are nonfunctional in one species may, in another organism, become an exon—a section of DNA that is eventually transcribed to messenger RNA. Izabela Makalowska of Pennsylvania State University recently showed that this mechanism quite often leads to another interesting feature in the vertebrate genomes, namely overlapping genes—that is, genes that share some of their nucleotides.
These and countless other examples demonstrate that repetitive elements are hardly "junk" but rather are important, integral components of eukaryotic genomes. Risking the personification of biological processes, we can say that evolution is too wise to waste this valuable information.

How to Deal with False Research Findings

February 27, 2007
The Science of Getting It Wrong: How to Deal with False Research Findings
The key may be for researchers to work closer and check one another's results
By JR Minkel

FALSE POSITIVES: Researchers poring over their samples for novel results may be contributing to a flood of false research results. Tighter collaboration between investigators may be one way to reduce such errors.

Talk about making waves. Two years ago medical researcher John Ioannidis of the University of Ioannina in Greece offered mathematical "proof" that most published research results are wrong. Now, statisticians using similar methods found—not surprisingly—that the more researchers reproduce a finding, the better chance it has of being true.
Another research team says researchers have to draw conclusions from imperfect information, but offers a way to draw the line between justified and unjustified risks.

Meantime, in a possible sign of change, some genetics researchers have begun working more closely in an effort to prevent errors and enhance the accuracy of their results.
In his widely read 2005 PLoS Medicine paper, Ioannidis, a clinical and molecular epidemiologist, attempted to explain why medical researchers must frequently repeal past claims. In the past few years alone, researchers have had to backtrack on the health benefits of low-fat, high-fiber diets and the value and safety of hormone replacement therapy as well as the arthritis drug Vioxx, which was pulled from the market after being found to cause heart attacks and strokes in high-risk patients.
Using simple statistics, without data about published research, Ioannidis argued that the results of large, randomized clinical trials—the gold standard of human research—were likely to be wrong 15 percent of the time and smaller, less rigorous studies are likely to fare even worse.
Among the most likely reasons for mistakes, he says: a lack of coordination by researchers and biases such as tending to only publish results that mesh with what they expected or hoped to find. Interestingly, Ioannidis predicted that more researchers in the field are not necessarily better—especially if they are overly competitive and furtive, like the fractured U.S. intelligence community, which failed to share information that might have prevented the September 11, 2001, terrorist strikes on the World Trade Center and the Pentagon.
But Ioannidis left out one twist: The odds that a finding is correct increase every time new research replicates the same result, according to a study published in the current PLoS Medicine. Lead study author Ramal Moonesinghe, a statistician at the Centers for Disease Control and Prevention, says that for simplicity's sake his group ignored the possibility that results can be replicated by repeating the same biases. The presence of bias reduces but does not erase the value of replication, he says.
"I fully agree that replication is key for improving credibility & replication is more important than discovery," Ioannidis says. But he adds that biases also have to be weeded out, otherwise replication may not be enough. For example, researchers reported in a much touted 2006 Science article that they had discovered a gene variant that seemed to confer a risk for obesity, and they replicated the results in four human populations. Last month, they acknowledged that the finding was probably wrong.
Ioannidis says that researchers have become increasingly sophisticated at acquiring large amounts of data from genomics and other studies, and at spinning it in different ways—much like TV weathercasters proclaiming every day a record-setting meteorological event of some sort. As a result, he says, it is easy to come up with findings that are "significant" in the statistical sense, yet not scientifically valid.
To deal with this poverty of riches, Ioannidis proposes that researchers cooperate more to confirm one another's findings Toward that end, he and other genetics researchers two years ago established a network of research consortia now consisting of 26 groups, he says, each with a dozen to hundreds of members, for investigators studying various cancers, HIV, Parkinson's disease and other disorders. The groups are intended to help teams in each field replicate one another's work.
Networks or not, doctors and health officials also have to decide how to treat patients based on published research that could be overturned, notes oncologist Benjamin Djulbegovic of the H. Lee Moffitt Cancer Center and Research Institute in Tampa. He and his colleagues contend in a second PLoS paper that physicians' decisions should be based on a mix of estimates of error for different types of studies (such as those that Ioannidis calculated), the potential benefits of the treatments reported in those studies, and how much of those benefits their patients can do without (or how much harm they can live with) if the finding turns out to be false.
"We can't work with 100 percent certainty," Djulbegovic says. "The question is: How false is false?" A well conducted randomized trial is more likely to produce correct results, but a less rigorous study might still satisfy a physician if the risks are low and its potential benefits are great, he says.
Ioannidis agrees that perfect certainty is impossible. "If you have a severe disease and there is only one medication available, and you know that it is only 5 percent likely to work, why not use it?" he says. But implementing such a calculus is trickier than it appears, he adds, because "we cannot assume that an intervention is necessarily safe in the absence of strong data testifying to this."

from Scientific American

on Spring Festival holiday！

on February 12th, 1809, a great man was born——CHARLES ROBERT DARWIN（February 12, 1809 to April 19, 1882）, So let's take a moment to ponder the central dogma of modern biology, best embodied by the title of a 1973 essay by evolutionary biologist (and Russian Orthodox Christian) Theodosius Dobzhansky:
Nothing in Biology Makes Sense Except in the Light of Evolution.

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!

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

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.

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

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

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!