2009年4月08日,，北京生命科學研究所張宏實驗室在Autophagy雜志上在線發(fā)表題為“Selective autophagic degradation of maternally-derived germline P granule components in somatic cells in C. elegans ”的文章,。
該文章指出在早期胚胎分裂過程中,，殘留在體細胞胞質中的有聚集傾向的P顆粒成分PGL-1和PGL-3通過自體吞噬作用被清除掉,。包括VPS-34/BEC-1復合體在內的自體吞噬相關蛋白失去功能后會導致體細胞中PGL-1和PGL-3聚集形成PGL顆粒,。這種PGL顆粒的形成是由SEPA-1介導的,。這種自體吞噬介導的選擇性降解蛋白聚合體在線蟲發(fā)育過程中有重要的生理作用,。
趙玉為該文章的第一作者，論文的其他作者還有本所的田娥,。張宏博士為本文的通訊作者,。該項研究由科技部863項目資助，在北京生命科學研究所完成,。（生物谷Bioon.com）
生物谷推薦原始出處：
Autophagy Volume 5, Issue 5 July 1, 2008
Selective autophagic degradation of maternally-loaded germline P granule components in somatic cells during C. elegans embryogenesis
Yu Zhao, E Tian and Hong Zhang
National Institute of Biological Sciences; Beijing, China
Germline P granules are specialized protein/RNA aggregates that are found exclusively in germ cells in C. elegans. During the early embryonic divisions that generate germ blastomeres, aggregate-prone P granule components PGL-1 and PGL-3 that remain in the cytoplasm destined for somatic daughters are selectively removed by autophagy. Loss-of-function of components of the autophagy pathway, including the VPS-34/BEC-1 complex, causes accumulation of PGL-1 and PGL-3 into aggregates in somatic cells (termed PGL granules). Formation of PGL granules depends on SEPA-1, which is an integral component of these granules. SEPA-1 is preferentially degraded by autophagy and is also required for the autophagic degradation of PGL-1 and PGL-3. SEPA-1 functions as a bridging molecule in mediating degradation of P granule components by directly interacting with PGL-3 and also with the autophagy protein LGG-1/Atg8. The defect in embryonic development in autophagy mutants is suppressed by mutation of sepa-1, suggesting that autophagic degradation of PGL granule components may provide nutrients for embryogenesis and/or also prevent the formation of aggregates that could be toxic for animal development. Our study reveals a specific physiological function of selective autophagic degradation during C. elegans development.
