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弓形虫棒状体蛋白ROP16通过指导p53的Ser15/37磷酸化部分介导SH-SY5Y细胞凋亡和细胞周期阻滞。

Toxoplasma gondii Rhoptry Protein ROP16 Mediates Partially SH-SY5Y Cells Apoptosis and Cell Cycle Arrest by Directing Ser15/37 Phosphorylation of p53.

作者信息

Chang Shuang, Shan Xiumei, Li Xingliang, Fan Weiwei, Zhang Steven Qian, Zhang Jin, Jiang Nan, Ma Duan, Mao Zuohua

机构信息

1. Department of Parasitology and Microbiology, School of Basic Medical Sciences, Fudan University, Shanghai, 200032, China.

2. Key Laboratory of Molecular Medicine, Ministry of Education, Department of Biochemistry and Molecular Biology, Institutes of Biomedical Sciences, School of Basic Medical Sciences, Fudan University, Shanghai, 200032, China.

出版信息

Int J Biol Sci. 2015 Aug 15;11(10):1215-25. doi: 10.7150/ijbs.10516. eCollection 2015.

DOI:10.7150/ijbs.10516
PMID:26327815
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4551757/
Abstract

Toxoplasma rhoptries, an unusual set of apical organelles that are associated with Toxoplasma infection may cause subversion of the host cell functions. Parasite rhoptry protein 16 (ROP16) is a regulator of host cell transcription during cell invasion in which it migrates into the host cell cytoplasm and subsequently localizes to the nucleus. In the present study, we found that overexpression of ROP16 could partially mediate human neuroblastoma SH-SY5Y apoptosis (12.47%) and cell cycle arrest in G1 phase (60.77%) in a p53 dependent manner by influencing the expression of Bax/Bcl-2 and p21/CDKs. ROP16 was identified to co-localize with p53, a novel direct interaction partner in the nucleus of SH-SY5Y. Furthermore, SH-SY5Y apoptosis via the mitochondria-dependent p53 pathway and cell cycle arrest caused by ROP16 dealt with direct serine 15/37 phosphorylation of p53. Our studies provide a new mechanism by which ROP16 interacts with the nucleus proteins which subsequently subverts the host cells functions.

摘要

弓形虫棒状体是一组与弓形虫感染相关的特殊顶端细胞器，可能导致宿主细胞功能的颠覆。寄生虫棒状体蛋白16（ROP16）是细胞入侵过程中宿主细胞转录的调节因子，在入侵过程中它迁移到宿主细胞胞质中，随后定位于细胞核。在本研究中，我们发现ROP16的过表达可通过影响Bax/Bcl-2和p21/CDKs的表达，以p53依赖的方式部分介导人神经母细胞瘤SH-SY5Y细胞凋亡（12.47%）和G1期细胞周期阻滞（60.77%）。ROP16被确定与p53共定位，p53是SH-SY5Y细胞核中的一种新型直接相互作用伙伴。此外，ROP16引起的通过线粒体依赖的p53途径的SH-SY5Y细胞凋亡和细胞周期阻滞涉及p53的直接丝氨酸15/37磷酸化。我们的研究提供了一种新机制，即ROP16与核蛋白相互作用，随后颠覆宿主细胞功能。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/958f/4551757/33ac7d06d414/ijbsv11p1215g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/958f/4551757/76df0f87a707/ijbsv11p1215g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/958f/4551757/f87fe720fe7f/ijbsv11p1215g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/958f/4551757/f08ec8e34c9d/ijbsv11p1215g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/958f/4551757/165b8fe7bda0/ijbsv11p1215g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/958f/4551757/db8a605d0006/ijbsv11p1215g005.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/958f/4551757/e72f8884fd7a/ijbsv11p1215g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/958f/4551757/313fe0623ade/ijbsv11p1215g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/958f/4551757/44e7345aab7c/ijbsv11p1215g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/958f/4551757/33ac7d06d414/ijbsv11p1215g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/958f/4551757/76df0f87a707/ijbsv11p1215g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/958f/4551757/f87fe720fe7f/ijbsv11p1215g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/958f/4551757/f08ec8e34c9d/ijbsv11p1215g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/958f/4551757/165b8fe7bda0/ijbsv11p1215g004.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/958f/4551757/c42bff836971/ijbsv11p1215g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/958f/4551757/e72f8884fd7a/ijbsv11p1215g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/958f/4551757/313fe0623ade/ijbsv11p1215g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/958f/4551757/44e7345aab7c/ijbsv11p1215g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/958f/4551757/33ac7d06d414/ijbsv11p1215g010.jpg

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