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Baumann Lab Defines Proteins that Distinguish Chromosome Ends from DNA Double-Strand Breaks
May 11, 2007Peter Baumann, Ph.D., Assistant Investigator, and Nancy Bae, Ph.D., Postdoctoral Research Associate in the Baumann Lab, have published a paper offering insight into the way cells protect chromosome ends from misguided repair.
Published in today's issue of Molecular Cell, their paper entitled "A RAP1/TRF2 Complex Inhibits Non-Homologous End Joining at Human Telomeric DNA Ends" employed a biochemical assay for double-strand break repair to define the minimal requirements for the protection of telomeric DNA at the ends of chromosomes.
"Surprisingly, we found that neither long single-stranded overhangs nor t-loop formation is essential to prevent illegitimate repair of telomeric ends," said Dr. Bae. "Instead, a short tandem array of telomeric repeats bound by a Rap1/Trf2 complex is sufficient to impede non-homologous end joining in a highly directional manner."
It has long been understood that chromosome ends are distinct from DNA double-strand breaks and that the cellular machinery that repairs DNA breaks does not act on telomeres. But how repair factors are prevented from acting at chromosome ends has been a hotly debated issue. Over the past decade, several telomeric complexes and structures have been identified and proposed to protect chromosome ends, but conclusive evidence that any of these are required for protection has been lacking.
"We set out to define the minimal requirements that would allow the DNA repair machinery to distinguish a chromosome end from a break," said Dr. Baumann. "By establishing an in vitro assay for chromosome end protection and by implicating specific proteins, we have opened the door to elucidate the mechanism by which RAP1/TRF2 inhibits double-strand break repair at chromosome ends."
"These findings are important for establishing a better understanding of tumor development," said Robb Krumlauf, Ph.D., Scientific Director. "Genomic instability and gross chromosomal rearrangements are a hallmark of cancer cells. The mechanisms that initiate and drive these events are only poorly understood, but it is widely accepted that loss of chromosome end protection can initiate genomic instability through bridge-breakage-fusion cycles. It is, therefore, very important to understand the mechanism of chromsome end protection and how and why it fails during tumorigenesis."
Dr. Baumann, who received a Pew Scholar Award in 2003 and a Basil O'Connor Scholar Award in 2004, holds an academic appointment as an Assistant Professor in the Department of Biochemistry & Molecular Biology at The University of Kansas School of Medicine. To learn more about the work of the Baumann Lab, visit http://www.stowers-institute.org/labs/BaumannLab.asp.
About the Stowers Institute
Housed in a 600,000 square-foot state-of-the-art facility on a 10-acre campus in the heart of Kansas City, Missouri, the Stowers Institute for Medical Research conducts basic research on fundamental processes of cellular life. Through its commitment to collaborative research and the use of cutting-edge technology, the Institute seeks more effective means of preventing and curing disease. The Institute was founded by Jim and Virginia Stowers, two cancer survivors who have created combined endowments of $2 billion in support of basic research of the highest quality.
Stowers Institute
It has long been understood that chromosome ends are distinct from DNA double-strand breaks and that the cellular machinery that repairs DNA breaks does not act on telomeres. But how repair factors are prevented from acting at chromosome ends has been a hotly debated issue. Over the past decade, several telomeric complexes and structures have been identified and proposed to protect chromosome ends, but conclusive evidence that any of these are required for protection has been lacking.
"We set out to define the minimal requirements that would allow the DNA repair machinery to distinguish a chromosome end from a break," said Dr. Baumann. "By establishing an in vitro assay for chromosome end protection and by implicating specific proteins, we have opened the door to elucidate the mechanism by which RAP1/TRF2 inhibits double-strand break repair at chromosome ends."
"These findings are important for establishing a better understanding of tumor development," said Robb Krumlauf, Ph.D., Scientific Director. "Genomic instability and gross chromosomal rearrangements are a hallmark of cancer cells. The mechanisms that initiate and drive these events are only poorly understood, but it is widely accepted that loss of chromosome end protection can initiate genomic instability through bridge-breakage-fusion cycles. It is, therefore, very important to understand the mechanism of chromsome end protection and how and why it fails during tumorigenesis."
Dr. Baumann, who received a Pew Scholar Award in 2003 and a Basil O'Connor Scholar Award in 2004, holds an academic appointment as an Assistant Professor in the Department of Biochemistry & Molecular Biology at The University of Kansas School of Medicine. To learn more about the work of the Baumann Lab, visit http://www.stowers-institute.org/labs/BaumannLab.asp.
About the Stowers Institute
Housed in a 600,000 square-foot state-of-the-art facility on a 10-acre campus in the heart of Kansas City, Missouri, the Stowers Institute for Medical Research conducts basic research on fundamental processes of cellular life. Through its commitment to collaborative research and the use of cutting-edge technology, the Institute seeks more effective means of preventing and curing disease. The Institute was founded by Jim and Virginia Stowers, two cancer survivors who have created combined endowments of $2 billion in support of basic research of the highest quality.
Stowers Institute
Chromosomes Current Events and Chromosomes News RSSPossible Link Studied Between Childhood Abuse and Early Cellular Aging
Children who suffer physical or emotional abuse may be faced with accelerated cellular aging as adults, according to new research from Butler Hospital and Brown University.
Scientists at UA, collaborating institutions decode maize genome
Scientists from the University of Arizona led by Arizona Genomics Institute director Rod A. Wing and from collaborating institutions have deciphered the complete genetic code of the maize plant for the first time.
New map of variation in maize genetics holds promise for developing new varieties
A new study of maize has identified thousands of diverse genes in genetically inaccessible portions of the genome. New techniques may allow breeders and researchers to use this genetic variation to identify desirable traits and create new varieties that were not easily possible before.
New Maize Map to Aid Plant Breeding Efforts
In a massive survey of genetic diversity in maize, also known as corn, researchers across the United States, have developed a gene map that should pave the way to significant improvements in a plant that is a major source of food, fuel, animal feed and fiber around the world.
Chromosomes dance and pair up on the nuclear membrane
Meiosis - the pairing and recombination of chromosomes, followed by segregation of half to each egg or sperm cell - is a major crossroads in all organisms reproducing sexually.
Largest gene study of childhood IBD identifies 5 new genes
In the largest, most comprehensive genetic analysis of childhood-onset inflammatory bowel disease (IBD), an international research team has identified five new gene regions, including one involved in a biological pathway that helps drive the painful inflammation of the digestive tract that characterizes the disease.
NIH-funded researchers transform embryonic stem cells into human germ cells
Researchers funded in part by the National Institutes of Health have discovered how to transform human embryonic stem cells into germ cells, the embryonic cells that ultimately give rise to sperm and eggs.
A solution to Darwin's 'mystery of the mysteries' emerges from the dark matter of the genome
Biological species are often defined on the basis of reproductive isolation. Ever since Darwin pointed out his difficulty in explaining why crosses between two species often yield sterile or inviable progeny (for instance, mules emerging from a cross between a horse and a donkey), biologists have struggled with this question.
Common weed could provide clues on aging and cancer
A common weed and human cancer cells could provide some very uncommon details about DNA structure and its relationship with telomeres and how they affect cellular aging and cancer, according to a team led by scientists from Texas A&M University and the University of Cincinnati (UC).
CSHL-led team discovers rare mutation dramatically increasing schizophrenia risk
An international team of researchers led by geneticist Jonathan Sebat, Ph.D., of Cold Spring Harbor Laboratory (CSHL), has identified a mutation on human chromosome 16 that substantially increases risk for schizophrenia.
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