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弓形虫通过磷酸化开关 I 使 Irgb6 失活的结构基础。

Structural basis of Irgb6 inactivation by Toxoplasma gondii through the phosphorylation of switch I.

机构信息

Division of Structural Medicine and Anatomy, Department of Physiology and Cell Biology, Kobe University Graduate School of Medicine, Kobe, Japan.

Department of Neuroscience, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University, Okayama, Japan.

出版信息

Genes Cells. 2024 Jan;29(1):17-38. doi: 10.1111/gtc.13080. Epub 2023 Nov 20.

Abstract

Irgb6 is a priming immune-related GTPase (IRG) that counteracts Toxoplasma gondii. It is known to be recruited to the low virulent type II T. gondii parasitophorous vacuole (PV), initiating cell-autonomous immunity. However, the molecular mechanism by which immunity-related GTPases become inactivated after the parasite infection remains obscure. Here, we found that Thr95 of Irgb6 is prominently phosphorylated in response to low virulent type II T. gondii infection. We observed that a phosphomimetic T95D mutation in Irgb6 impaired its localization to the PV and exhibited reduced GTPase activity in vitro. Structural analysis unveiled an atypical conformation of nucleotide-free Irgb6-T95D, resulting from a conformational change in the G-domain that allosterically modified the PV membrane-binding interface. In silico docking corroborated the disruption of the physiological membrane binding site. These findings provide novel insights into a T. gondii-induced allosteric inactivation mechanism of Irgb6.

摘要

Irgb6 是一种初始免疫相关 GTPase(IRG),可抵抗刚地弓形虫。已知它被招募到低毒力 II 型刚地弓形虫寄生空泡(PV),启动细胞自主免疫。然而,寄生虫感染后免疫相关 GTPase 失活的分子机制仍不清楚。在这里,我们发现 Irgb6 的 Thr95 在响应低毒力 II 型刚地弓形虫感染时明显发生磷酸化。我们观察到 Irgb6 中的 Thr95D 磷酸模拟突变会损害其在 PV 上的定位,并表现出体外 GTPase 活性降低。结构分析揭示了 Irgb6-T95D 无核苷酸的非典型构象,这是由于 G 结构域的构象变化,从而改变了 PV 膜结合界面的变构。计算机对接证实了破坏了生理膜结合位点。这些发现为刚地弓形虫诱导的 Irgb6 变构失活机制提供了新的见解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/21fd/11448365/2bd0660ff037/GTC-29-17-g002.jpg

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