2009年4月08日，北京生命科学研究所张宏实验室在Autophagy杂志上在线发表题为“Selective autophagic degradation of maternally-derived germline P granule components in somatic cells in C. elegans ”的文章。
该文章指出在早期胚胎分裂过程中，残留在体细胞胞质中的有聚集倾向的P颗粒成分PGL-1和PGL-3通过自体吞噬作用被清除掉。包括VPS-34/BEC-1复合体在内的自体吞噬相关蛋白失去功能后会导致体细胞中PGL-1和PGL-3聚集形成PGL颗粒。这种PGL颗粒的形成是由SEPA-1介导的。这种自体吞噬介导的选择性降解蛋白聚合体在线虫发育过程中有重要的生理作用。
赵玉为该文章的第一作者，论文的其他作者还有本所的田娥。张宏博士为本文的通讯作者。该项研究由科技部863项目资助，在北京生命科学研究所完成。（生物谷Bioon.com）
生物谷推荐原始出处：
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.
