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Human RecQ helicases, homologous recombination and genomic instability
November 15, 2007Two independent papers in the December 1st issue of G&D detail how human RecQ helicases regulate homologous recombination and protect genome stability.
The human RecQ family of helicases consists of 5 members: WRN, BLM, RECQL4, RECQL1 and RECQL5. These enzymes help to unwind DNA so to facilitate replication, transcription and DNA repair. Mutations in BLM, WRN and RECQ4 cause the cancer-predisposition syndromes Bloom's Syndrome, Werner's Syndrome and Rothmund-Thomson Syndrome, respectively. Interestingly, these cancer-prone genetic conditions are associated with defects in the DNA repair pathway of homologous recombination (HR).
Dr. Alexander Mazin (Drexel University College of Medicine) and colleagues focused their research on the function of the Bloom's syndrome helicase, BLM. They found that BLM has differential roles in regulating HR: depending upon the stage of its involvement, BLM can either promote or inhibit HR - leading the authors to the surprising conclusion that the "combination of opposing activities gives BLM an important leverage in regulation of HR."
In a separate paper, Drs. Guangbin Luo (Case Western Reserve Univeristy) and Patrick Sung (Yale University School of Medicine) and their colleagues demonstrate that another member of the human RecQ family, RECQL5, can also interfere with HR, by disrupting a particular step (formation of the Rad51 presynaptic filament) in the pathway. Dr. Sung emphasizes that "These results elucidate hoe RECQL5 proetin helps avoid deleterious chromosome rearrangements that can cause tumorigenesis."
Taken together, these papers lend new insight into the molecular function of human RecQ helicases in protecting genome stability and preventing tumorigenesis.
Cold Spring Harbor Laboratory
In a separate paper, Drs. Guangbin Luo (Case Western Reserve Univeristy) and Patrick Sung (Yale University School of Medicine) and their colleagues demonstrate that another member of the human RecQ family, RECQL5, can also interfere with HR, by disrupting a particular step (formation of the Rad51 presynaptic filament) in the pathway. Dr. Sung emphasizes that "These results elucidate hoe RECQL5 proetin helps avoid deleterious chromosome rearrangements that can cause tumorigenesis."
Taken together, these papers lend new insight into the molecular function of human RecQ helicases in protecting genome stability and preventing tumorigenesis.
Cold Spring Harbor Laboratory
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Environmental triggers may promote human genetic variation
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Researchers gain free access to industry-owned key patents in molecular biology
Ascenion mediates licence agreements with Cellectis and DuPont Munich, 1st June, 2004 - Ascenion GmbH has established for the first time a clear legal basis whereby the research institutions DKFZ, GBF, GSF and MDC may use key technologies for which Cellectis SA and DuPont together with Bristol-Myers Squibb have dominant patent positions. The technologies are homologous recombination (Cellectis) and the Cre-Lox system (DuPont and Bristol-Myers Squibb respectively) - fundamental molecular biology techniques widely used to investigate the function and regulation of individual genes. An important area of application for these techniques are so-called knock-out mice that are indispensable in bot
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