Menstruation Research Today is a free monthly online journal that collates and summarizes the latest research about Menstruation, including details on menstrual cycle, pregnancy, pain, irregular menstruation. | ||||||||
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Mice deficient in oocyte-specific oligoadenylate synthetase-like protein OAS1D display reduced fertility.Yan W, Ma L, Stein P, Pangas SA, Burns KH, Bai Y, Schultz RM, Matzuk MM Department of Pathology, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA. The double-stranded RNA (dsRNA)-induced interferon response is a defense mechanism against viral infection. Upon interferon activation by dsRNA, 2',5'-oligoadenylate synthetase 1 (OAS1A) is induced; it binds dsRNA and converts ATP into 2',5'-linked oligomers of adenosine (called 2-5A), which activate RNase L that in turn degrades viral and cellular RNAs. In a screen to identify oocyte-specific genes, we identified a novel murine cDNA encoding an ovary-specific 2',5'-oligoadenylate synthetase-like protein, OAS1D, which displays 59% identity with OAS1A. OAS1D is predominantly cytoplasmic and is exclusively expressed in growing oocytes and early embryos. Like OAS1A, OAS1D binds the dsRNA mimetic poly(I-C), but unlike OAS1A, it lacks 2'-5' adenosine linking activity. OAS1D interacts with OAS1A and inhibits the enzymatic activity of OAS1A. Mutant mice lacking OAS1D (Oas1d(-/-)) display reduced fertility due to defects in ovarian follicle development, decreased efficiency of ovulation, and eggs that are fertilized arrest at the one-cell stage. These effects are exacerbated after activation of the interferon/OAS1A/RNase L pathway by poly(I-C). We propose that OAS1D suppresses the interferon/OAS/RNase L-mediated cellular destruction by interacting with OAS1A during oogenesis and early embryonic development. Published 18 May 2005 in Mol Cell Biol, 25(11): 4615-24.
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