拟南芥 PMK-1/p38 MAPK 在秀丽隐杆线虫对鼠疫耶尔森氏菌感染的组织特异性免疫反应中是保守所必需的。
A conserved PMK-1/p38 MAPK is required in caenorhabditis elegans tissue-specific immune response to Yersinia pestis infection.
机构信息
Department of Molecular Genetics and Microbiology, Duke University Medical Center, Durham, North Carolina 27710, USA.
出版信息
J Biol Chem. 2010 Apr 2;285(14):10832-40. doi: 10.1074/jbc.M109.091629. Epub 2010 Feb 4.
Abstract
Yersinia pestis has acquired a variety of complex strategies that enable the bacterium to overcome defenses in different hosts and ensure its survival and successful transmission. A full-genome microarray analysis on Caenorhabditis elegans infected with Y. pestis shows enrichment in genes that are markers of innate immune responses and regulated by a conserved PMK-1/p38 MAPK. Consistent with a role in regulating expression of immune effectors, inhibition of PMK-1/p38 by mutation or RNA interference enhances susceptibility to Y. pestis. Further studies of mosaic animals where PMK-1/p38 is exclusively inhibited or overexpressed in a tissue-specific manner indicate that PMK-1/p38 controls expression of a CUB-like family of immune genes at the cell-autonomous level. Given the conserved nature of PMK-1/p38 MAPK-mediated signaling and innate immune responses, PMK-1/p38 MAPK may play a role in the immune response against Y. pestis in natural hosts.
摘要
鼠疫耶尔森菌已经获得了多种复杂的策略，使细菌能够克服不同宿主中的防御机制，确保其存活和成功传播。对感染鼠疫耶尔森菌的秀丽隐杆线虫进行的全基因组微阵列分析表明，与先天免疫反应相关的基因标记显著富集，并受保守的 PMK-1/p38 MAPK 调控。PMK-1/p38 抑制突变或 RNA 干扰增强了对鼠疫耶尔森菌的易感性，这与调节免疫效应子表达的作用一致。对镶嵌动物的进一步研究表明，PMK-1/p38 以组织特异性的方式被特异性抑制或过表达，表明 PMK-1/p38 在细胞自主水平上控制着 CUB 样免疫基因家族的表达。鉴于 PMK-1/p38 MAPK 介导的信号转导和先天免疫反应的保守性质，PMK-1/p38 MAPK 可能在天然宿主针对鼠疫耶尔森菌的免疫反应中发挥作用。
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