3月26日,，中科院生物物理研究所歐光朔研究組在《細胞生物學雜志》（Journal of Cell Biology）上在線發(fā)表題為Autophagy genes function sequentially to promote apoptotic cell corpse degradation in the engulfing cell的論文，報道了自體吞噬基因在吞噬細胞中發(fā)揮作用，促進凋亡細胞的降解,。
凋亡細胞的清除是細胞死亡的最終環(huán)節(jié)，其異常會導致炎癥和自身免疫紊亂,。細胞自體吞噬作用是指胞內(nèi)囊泡包裹胞質(zhì)中的內(nèi)含物運送到溶酶體中進行清除的過程,。前人研究表明，自體吞噬基因在細胞凋亡過程中發(fā)揮功能,，促進凋亡細胞產(chǎn)生被吞噬細胞識別所需的信號,。
這項新的研究以線蟲Q神經(jīng)前體細胞發(fā)育產(chǎn)生的凋亡細胞為模型，發(fā)現(xiàn)自體吞噬基因atg-18和epg-5并不在凋亡細胞中起作用,，而是在吞噬細胞中發(fā)揮功能,；自體吞噬蛋白在吞噬細胞中被招募到凋亡細胞表面，調(diào)控內(nèi)涵體和溶酶體與凋亡Q細胞的融合,，促進凋亡Q細胞的降解,。該發(fā)現(xiàn)拓展了人們在自體吞噬基因調(diào)控細胞凋亡方面的認識。
為了研究自體吞噬蛋白和其他蛋白被招募到凋亡細胞上的時序關系,，歐光朔研究組改造了一種藍色熒光蛋白（TagBFP）,，使之適用與線蟲，與GFP和mCherry共同使用,，實現(xiàn)了在線蟲中的三色熒光活體時序成像,。（生物谷 bioon.com）
doi:doi: 10.1083/jcb.201111053
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Autophagy genes function sequentially to promote apoptotic cell corpse degradation in the engulfing cell
Wei Li, Wei Zou, Yihong Yang, Yongping Chai, Baohui Chen, Shiya Cheng, Dong Tian, Xiaochen Wang, Ronald D. Vale，Guangshuo Ou
Apoptotic cell degradation is a fundamental process for organism development, and impaired clearance causes inflammatory or autoimmune disease. Although autophagy genes were reported to be essential for exposing the engulfment signal on apoptotic cells, their roles in phagocytes for apoptotic cell removal are not well understood. In this paper, we develop live-cell imaging techniques to study apoptotic cell clearance in the Caenorhabditis elegans Q neuroblast lineage. We show that the autophagy proteins LGG-1/LC3, ATG-18, and EPG-5 were sequentially recruited to internalized apoptotic Q cells in the phagocyte. In atg-18 or epg-5 mutants, apoptotic Q cells were internalized but not properly degraded; this phenotype was fully rescued by the expression of autophagy genes in the phagocyte. Time-lapse analysis of autophagy mutants revealed that recruitment of the small guanosine triphosphatases RAB-5 and RAB-7 to the phagosome and the formation of phagolysosome were all significantly delayed. Thus, autophagy genes act within the phagocyte to promote apoptotic cell degradation.
