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干扰素诱导免疫相关 GTP 酶 Irgm1(LRG-47)在小鼠细胞中的定位和错误定位。

Localisation and mislocalisation of the interferon-inducible immunity-related GTPase, Irgm1 (LRG-47) in mouse cells.

机构信息

Institute for Genetics, University of Cologne, Cologne, Germany.

出版信息

PLoS One. 2010 Jan 13;5(1):e8648. doi: 10.1371/journal.pone.0008648.

Abstract

Irgm1 (LRG-47) is an interferon-inducible Golgi membrane associated GTPase of the mouse whose disruption causes susceptibility to many different intracellular pathogens. Irgm1 has been variously interpreted as a regulator of homologous effector GTPases of the IRG family, a regulator of phagosome maturation and as an initiator of autophagy in interferon-induced cells. We find that endogenous Irgm1 localises to late endosomal and lysosomal compartments in addition to the Golgi membranes. The targeting motif known to be required for Golgi localisation is surprisingly also required for endolysosomal localisation. However, unlike Golgi localisation, localisation to the endolysosomal system also requires the functional integrity of the nucleotide binding site, and thus probably reflects transient activation. Golgi localisation is lost when Irgm1 is tagged at either N- or C-termini with EGFP, while localisation to the endolysosomal system is relatively favoured. N-terminally tagged Irgm1 localises predominantly to early endosomes, while C-terminally tagged Irgm1 localises to late endosomes and lysosomes. Both these anomalous distributions are reversed by inactivation of the nucleotide binding site, and the tagged proteins both revert to Golgi membrane localisation. Irgm1 is the first IRG protein to be found associated with the endolysosomal membrane system in addition to either Golgi (Irgm1 and Irgm2) or ER (Irgm3) membranes, and we interpret the result to be in favour of a regulatory function of IRGM proteins at cellular membrane systems. In future analyses it should be borne in mind that tagging of Irgm1 leads to loss of Golgi localisation and enhanced localisation on endolysosomal membranes, probably as a result of constitutive activation.

摘要

Irgm1(LRG-47)是一种干扰素诱导的高尔基体膜相关 GTPase,其缺失会导致对许多不同的细胞内病原体的易感性。Irgm1 被不同地解释为 IRG 家族同源效应物 GTPase 的调节剂、吞噬体成熟的调节剂以及干扰素诱导细胞中自噬的起始因子。我们发现内源性 Irgm1 除了高尔基体膜外,还定位于晚期内体和溶酶体区室。已知对于高尔基体定位所必需的靶向基序也出人意料地需要内体溶酶体定位。然而,与高尔基体定位不同,内体溶酶体系统的定位还需要核苷酸结合位点的功能完整性,因此可能反映了瞬时激活。当 Irgm1 的 N 或 C 末端用 EGFP 标记时,高尔基体定位会丢失,而内体溶酶体系统的定位相对更有利。N 末端标记的 Irgm1 主要定位于早期内体,而 C 末端标记的 Irgm1 定位于晚期内体和溶酶体。这两种异常分布都被核苷酸结合位点的失活所逆转,并且标记的蛋白质都恢复到高尔基体膜定位。Irgm1 是除了高尔基体(Irgm1 和 Irgm2)或内质网(Irgm3)膜之外,第一个与内体溶酶体膜系统相关的 IRG 蛋白,我们的解释是 IRGM 蛋白在细胞膜系统中具有调节功能。在未来的分析中,应该记住 Irgm1 的标记会导致高尔基体定位的丧失和内体溶酶体膜定位的增强,可能是由于组成型激活。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ebfb/2799677/0e0e9002e312/pone.0008648.g001.jpg

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