Reports outline biochemistry research from Tohoku University
2007 JUN 19 -- Data detailed in "Activation of a novel pathway involving Mms1 and Rad59 in sgs1 cells" have been presented. According to recent research published in the journal Biochemical and Biophysical Research Communications, "Unequal sister chromatid recombination (uSCR) is elevated in budding yeast sgs1 mutants, which lack a homolog of the human BLM gene that causes Bloom syndrome. Examination of the mechanism responsible for elevated uSCR in sgs1 mutants showed that mutation of RAD51 also resulted in hyper-uSCR." "Data from this study show that defects in the Rad51-Sgs1-dependent and Sgs1-dependent lesion-bypass pathways activate Rad59-Rad1-and Rad59-dependent pathways, respectively, resulting in uSCR. Moreover, the elevation of uSCR in sgs1 and rad51 mutants was dependent on MMS1, which encodes one of the components of the Mms22 module," wrote A. Ui and colleagues, Tohoku University. The researchers concluded: "Lastly, a putative role of Mms1 in the elevation of uSCR and a possible mechanism by which uSCR is elevated as a result of defective Sgs1 and Rad51 are discussed." Ui and colleagues published their study in Biochemical and Biophysical Research Communications (Activation of a novel pathway involving Mms1 and Rad59 in sgs1 cells. Biochemical and Biophysical Research Communications, 2007;356(4):1031-7). For additional information, contact A. Ui, Molecular Cell Biology Laboratory, Graduate School of Pharmaceutical Sciences, Tohoku University, Aoba 6-3, Aramaki, Aoba-ku, Sendai 980-8578, Japan. The publisher's contact information for the journal Biochemical and Biophysical Research Communications is: Academic Press Inc. Elsevier Science, 525 B St., Ste. 1900, San Diego, CA 92101-4495, USA. Keywords: Japan, Sendai, Biochemistry, Biochemical. This article was prepared by Life Science Weekly editors from staff and other reports. Copyright 2007, Life Science Weekly via NewsRx.com.
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