生物谷報道：我們知道脊椎動物的卵子都會隨著年齡增加而逐漸減少,，最終消失,，從而失去繁殖或生育能力,。但為什么會隨年齡增長而消失呢？最新一期Cell封面文章揭示了其中的奧秘,。Nutt等發(fā)現(xiàn),，卵細(xì)胞的能量代謝是核心因素，通過能量代謝,，從而活化了CaMKII,，從而介導(dǎo)caspase-2的活化，導(dǎo)致了卵細(xì)胞凋亡,。這一研究成果首次將細(xì)胞代謝與卵細(xì)胞生存聯(lián)系在一起,，這雌性生殖能力的調(diào)控提供了新的思路。
Vertebrate female reproduction is limited by the oocyte stockpiles acquired during embryonic development. These are gradually depleted over the organism’s lifetime through the process of apoptosis. The timer that triggers this cell death is yet to be identified. We used the Xenopus egg/oocyte system to examine the hypothesis that nutrient stores can regulate oocyte viability. We show that pentose-phosphate-pathway generation of NADPH is critical for oocyte survival and that the target of this regulation is caspase-2, previously shown to be required for oocyte death in mice. Pentose-phosphate-pathway-mediated inhibition of cell death was due to the inhibitory phosphorylation of caspase-2 by calcium/calmodulin-dependent protein kinase II (CaMKII). These data suggest that exhaustion of oocyte nutrients, resulting in an inability to generate NADPH, may contribute to ooctye apoptosis. These data also provide unexpected links between oocyte metabolism, CaMKII, and caspase-2.
原文來源：L.K. Nutt, S.S. Margolis, M. Jensen, C.E. Herman, W.G. Dunphy, J.C. Rathmell, and S. Kornbluth Metabolic Regulation of Oocyte Cell Death through the CaMKII-Mediated Phosphorylation of Caspase-2. Cell, Volume 122, Issue 6. September 23, 2005
