Neuronal Goα and CAPS regulate behavioral and immune responses to bacterial pore-forming toxins.

Neuronal Goα and CAPS regulate behavioral and immune responses to bacterial pore-forming toxins.
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DOI:
10.1371/journal.pone.0054528
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发表时间:
2013
期刊:
影响因子:
3.7
通讯作者:
Aroian RV
Aroian RV
中科院分区:
综合性期刊3区
文献类型:
--
作者:
Los FC;Ha C;Aroian RV

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致孔性毒素(PFT)是一类攻击宿主细胞膜的丰富的细菌毒力因子。到目前为止,宿主对PFT的防御机制描述了宿主组织中直接受到PFT攻击的所有功能。在这里,我们描述了一种对PFT攻击的快速和完全穿透性的停止摄食秀丽线虫的反应。我们通过对线虫突变体的分析证明,通过PFT抑制取食需要神经元G蛋白Goα亚单位GOA-1,而维持这种反应需要神经元表达的蛋白分泌钙激活剂(CAPS)同系物UNC-31。独立于它们在停止摄食中的作用,我们发现GOA-1和UNC-31对于针对PFTs的免疫保护是额外需要的。因此,我们证明了对细菌PFT攻击的行为和免疫反应涉及神经系统和直接受到攻击的细胞之间的串扰。
Pore-forming toxins (PFTs) are abundant bacterial virulence factors that attack host cell plasma membranes. Host defense mechanisms against PFTs described to date all function in the host tissue that is directly attacked by the PFT. Here we characterize a rapid and fully penetrant cessation of feeding of Caenorhabditis elegans in response to PFT attack. We demonstrate via analyses of C. elegans mutants that inhibition of feeding by PFT requires the neuronal G protein Goα subunit goa-1, and that maintenance of this response requires neuronally expressed calcium activator for protein secretion (CAPS) homolog unc-31. Independently from their role in feeding cessation, we find that goa-1 and unc-31 are additionally required for immune protection against PFTs. We thus demonstrate that the behavioral and immune responses to bacterial PFT attack involve the cross-talk between the nervous system and the cells directly under attack.
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