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DNA 修复、抗原变异、细胞黏附和机会在生存中的整合:一个视角。

Integration of DNA Repair, Antigenic Variation, Cytoadhesion, and Chance in Survival: A Perspective.

机构信息

Department of Infectious Diseases and Immunology, University of Florida, Gainesville, FL, United States.

Genetics Institute, University of Florida, Gainesville, FL, United States.

出版信息

Front Cell Infect Microbiol. 2022 Apr 14;12:869696. doi: 10.3389/fcimb.2022.869696. eCollection 2022.

DOI:10.3389/fcimb.2022.869696
PMID:35493746
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9047050/
Abstract

Apicomplexan parasites live in hostile environments in which they are challenged chemically and their hosts attempt in many ways to kill them. In response, the parasites have evolved multiple mechanisms that take advantage of these challenges to enhance their survival. Perhaps the most impressive example is the evolutionary co-option of DNA repair mechanisms by the parasites as a means to rapidly manipulate the structure, antigenicity, and expression of the products of specific multigene families. The purpose of variant proteins that mediate cytoadhesion has long been thought to be primarily the avoidance of splenic clearance. Based upon known biology, I present an alternative perspective in which it is survival of the oxidative environment within which spp. parasites live that has driven integration of DNA repair, antigenic variation, and cytoadhesion, and speculate on how genome organization affects that integration. This perspective has ramifications for the development of parasite control strategies.

摘要

顶复门寄生虫生活在充满敌意的环境中,它们在这些环境中面临着化学挑战,而宿主则试图通过多种方式杀死它们。为了应对这些挑战,寄生虫进化出了多种机制,以提高它们的生存能力。也许最令人印象深刻的例子是寄生虫对 DNA 修复机制的进化性共适应,将其作为一种快速操纵特定多基因家族产物的结构、抗原性和表达的手段。介导细胞黏附的变异蛋白的目的长期以来一直被认为主要是避免脾脏清除。基于已知的生物学,我提出了一个替代观点,即在 spp. 寄生虫生活的氧化环境中,生存是驱动 DNA 修复、抗原变异和细胞黏附的驱动力,并推测基因组组织如何影响这种整合。这种观点对寄生虫控制策略的发展具有重要意义。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6606/9047050/bc304c2c215b/fcimb-12-869696-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6606/9047050/bc304c2c215b/fcimb-12-869696-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6606/9047050/bc304c2c215b/fcimb-12-869696-g001.jpg

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Comp Immunol Microbiol Infect Dis. 2020 May 30;71:101503. doi: 10.1016/j.cimid.2020.101503.
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