Every day tiny segments of our DNA are chipped or fragmented or get stuck together when they should really be pulled apart. But what our genome necessarily lacks in stability it makes up for with a phalanx of guards that monitor and repair the damage.
In new research in the journal Science, researchers at Rockefeller University and Harvard Medical School have pinpointed the role that two well-known proteins play in the repair of one of the most lethal types of DNA damage. The damage, known as inter-strand crosslinks, occurs when the two strands of the double helix are linked together, blocking replication and transcription.
"Our cells encounter, on average, 10 inter-strand crosslinks a day," says Agata Smogorzewska, head of the Laboratory of Genome Maintenance at Rockefeller University. "We suspected that these two proteins directly participated in the repair process. Until now, we knew that they localized to the sites of damage but we had no idea what they were doing there. This work breaks that barrier."
Science & Technology
Performance enhancers are the currency of a competitive society. But there's one that we have always had: For millions of years, segments of our DNA have improved the performance of our genome, revving up protein production at those times we need it most. New research from Rockefeller University and the University of Michigan Medical School now show that these genome enhancers regulate how our bodies make germ-fighting antibodies, molecules that keep savvy viruses and bacteria at bay.
The research, which appears this month in the Journal of Experimental Medicine, represents a major technological advance that will allow scientists to understand the role of enhancers in the immune system -- work that has stymied researchers for decades. "Many people left the field because working with antibody enhancers was so difficult," says F. Nina Papavasiliou, head of the Laboratory of Lymphocyte Biology at Rockefeller. "It seemed like there was no way around the problem."
Enhancers are short swaths of DNA that regulate genes from a distance, often megabases away. Generally, this distance from the genes they regulate makes enhancers hard to study. But immunoglobulin enhancers have been particularly problematic because of an additional twist: they are close to chromosome ends, which makes altering their local sequence especially difficult.
The research, which appears this month in the Journal of Experimental Medicine, represents a major technological advance that will allow scientists to understand the role of enhancers in the immune system -- work that has stymied researchers for decades. "Many people left the field because working with antibody enhancers was so difficult," says F. Nina Papavasiliou, head of the Laboratory of Lymphocyte Biology at Rockefeller. "It seemed like there was no way around the problem."
Enhancers are short swaths of DNA that regulate genes from a distance, often megabases away. Generally, this distance from the genes they regulate makes enhancers hard to study. But immunoglobulin enhancers have been particularly problematic because of an additional twist: they are close to chromosome ends, which makes altering their local sequence especially difficult.
© Unknown
New data has revealed that the heliosphere, the protective shield of energy that surrounds our solar system, has weakened by 25 per cent over the past decade and is now at it lowest level since the space race began 50 years ago.
Scientists are baffled at what could be causing the barrier to shrink in this way and are to launch mission to study the heliosphere.
The Interstellar Boundary Explorer, or IBEX, will be launched from an aircraft on Sunday on a Pegasus rocket into an orbit 150,000 miles above the Earth where it will "listen" for the shock wave that forms as our solar system meets the interstellar radiation.
Dr Nathan Schwadron, co-investigator on the IBEX mission at Boston University, said: "The interstellar medium, which is part of the galaxy as a whole, is actually quite a harsh environment. There is a very high energy galactic radiation that is dangerous to living things.
The annual Quadrantid meteor shower peaks on Jan. 3rd around 1900 UT (2 pm EST) when Earth passes through a stream of debris from shattered comet 2003 EH1. The timing of this northern shower favors observers in eastern Europe and Asia. Bright moonlight will interfere with the display, which can reach 100+ meteors per hour under ideal conditions.
In North America, where the peak occurs in daylight, it may be possible to hear the shower on meteor radar. Tune into Space Weather Radio for live echoes.
In North America, where the peak occurs in daylight, it may be possible to hear the shower on meteor radar. Tune into Space Weather Radio for live echoes.
The Solar and Heliospheric Observatory (SOHO) is tracking a comet that is about to make a perilous close approach to the sun.
Will the icy visitor survive? Click here for the latest image.
The comet was discovered by Australian amateur astronomer Alan Watson in images taken by NASA's STEREO-A spacecraft.
© SOHO
The comet was discovered by Australian amateur astronomer Alan Watson in images taken by NASA's STEREO-A spacecraft.
Nazdrovia! Nothing like starting off 2010 with a little talk of Armageddon (the movie). Rumors were flying around the Internet just before the New Year that the Russians are planning a mission to divert the asteroid 99942 Apophis away from Earth collision.
Comment: 2029? How about the other NEO's that can come at any time? Sounds like they are practicing for something sooner!
© Rockefeller University
All ears. Electron micrographs of two hair cell bundles in the zebra fish ear show the difference between those born with (left) and without (right) the protein Tmie.
All ears. Electron micrographs of two hair cell bundles in the zebra fish ear show the difference between those born with (left) and without (right) the protein Tmie.
"These zebrafish larvae were originally pegged for another study, but then we saw that one-fourth of them failed to respond to acoustic stimuli and made erratic spiraling movements,
and that suggested that they were born deaf," says first author Michelle R. Gleason, who spearheaded the project. "So we took this opportunity to examine what could be responsible for this extreme hearing loss."
At first, Gleason and Hudspeth, head of the Laboratory of Sensory Neuroscience and a Howard Hughes Medical Institute investigator, didn't detect any structural defects in the zebra fish's inner ear, which houses sound sensors called hair cells.
In the harsh judgment of natural selection, the ultimate measure of success is reproduction. So it's no surprise that life spends lavish resources on this feat, whether in the courtship behavior of birds and bees or replicating the cells that keep them alive. Now research has identified a new piece in an elaborate system to help guarantee fidelity in the reproduction of cells, preventing potentially lethal mutations in the process.
In experiments to be published in the December 18 issue of the Journal of Biological Chemistry, researchers at The Rockefeller University identified the molecule SMARCAL1 as part of cells' damage control response to malfunctioning DNA replication. In typical cell division, many different molecules have roles in guaranteeing the daughter strands of DNA are as identical as possible to their parent.
Some molecules check for errors or 'proofread' the offspring for typos, for instance; others, when alerted to a problem, arrest the replication process and conduct repairs.
In experiments to be published in the December 18 issue of the Journal of Biological Chemistry, researchers at The Rockefeller University identified the molecule SMARCAL1 as part of cells' damage control response to malfunctioning DNA replication. In typical cell division, many different molecules have roles in guaranteeing the daughter strands of DNA are as identical as possible to their parent.
Some molecules check for errors or 'proofread' the offspring for typos, for instance; others, when alerted to a problem, arrest the replication process and conduct repairs.
© DirecTV
Next year certainly will be big for the television and besides the huge screen HDTVs getting bit cheaper, we'll have first 3D channel. DirecTV, a U.S.-based TV service provider, is pondering to launch first 3D channel at the Consumer Electronic Show 2010 starting next week. At CES 2009, several companies like LG, Panasonic, Sony, Samsung, TCL/RCA, and Soyo/Honeywell demonstrated next generation 3D HDTV Panels.
HDGuru reported that DirecTV is planning to launch a 3D channel that offers content mix of content recorded in 3D HD. The company expects to start broadcasting in March once their satellite launches in orbit successfully. However, consumers will have to buy 3D HD supporting to watch this 3D HD content. At this moment, the flat panel 3D HDTVs are in production for several TV manufacturers.
For the 3D experience, one would need the 3D glasses just like the ones used in Nvidia GeForce 3D Vision.
Scientists have uncovered new evidence suggesting that damage to nerve cells in people with multiple sclerosis accumulates because the body's natural mechanism for repair of the nerve coating called "myelin" stalls out.
The study, published July 1, 2009, in the print edition of Genes & Development, was conducted by scientists at the University of California, San Francisco and University of Cambridge. The research was led by co-senior investigator David Rowitch, MD, PhD, a Howard Hughes Medical Institute investigator at UCSF.
The investigation, conducted in mice and in human tissue, showed that repair of nerve fibers is hampered by biochemical signals that inhibit the development of cells known as oligodendrocytes, which function as repair workers in the brain.
The study, published July 1, 2009, in the print edition of Genes & Development, was conducted by scientists at the University of California, San Francisco and University of Cambridge. The research was led by co-senior investigator David Rowitch, MD, PhD, a Howard Hughes Medical Institute investigator at UCSF.
The investigation, conducted in mice and in human tissue, showed that repair of nerve fibers is hampered by biochemical signals that inhibit the development of cells known as oligodendrocytes, which function as repair workers in the brain.
Comment: Chemo Does Not Cure: Often It Inflicts Damage and Spreads Cancer