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裂殖酵母中的 AP-1 辅助蛋白 Sip1 对于 Rho3 GTPase 的定位是必需的。

Sip1, an AP-1 accessory protein in fission yeast, is required for localization of Rho3 GTPase.

机构信息

Laboratory of Molecular Pharmacogenomics, School of Pharmaceutical Sciences, Kinki University, Kowakae, Higashi-Osaka, Japan.

出版信息

PLoS One. 2013 Jul 1;8(7):e68488. doi: 10.1371/journal.pone.0068488. Print 2013.

Abstract

Rho family GTPases act as molecular switches to regulate a range of physiological functions, including the regulation of the actin-based cytoskeleton, membrane trafficking, cell morphology, nuclear gene expression, and cell growth. Rho function is regulated by its ability to bind GTP and by its localization. We previously demonstrated functional and physical interactions between Rho3 and the clathrin-associated adaptor protein-1 (AP-1) complex, which revealed a role of Rho3 in regulating Golgi/endosomal trafficking in fission yeast. Sip1, a conserved AP-1 accessory protein, recruits the AP-1 complex to the Golgi/endosomes through physical interaction. In this study, we showed that Sip1 is required for Rho3 localization. First, overexpression of rho3⁺ suppressed defective membrane trafficking associated with sip1-i4 mutant cells, including defects in vacuolar fusion, Golgi/endosomal trafficking and secretion. Notably, Sip1 interacted with Rho3, and GFP-Rho3, similar to Apm1-GFP, did not properly localize to the Golgi/endosomes in sip1-i4 mutant cells at 27°C. Interestingly, the C-terminal region of Sip1 is required for its localization to the Golgi/endosomes, because Sip1-i4-GFP protein failed to properly localize to Golgi/endosomes, whereas the fluorescence of Sip1ΔN mutant protein co-localized with that of FM4-64. Consistently, in the sip1-i4 mutant cells, which lack the C-terminal region of Sip1, binding between Apm1 and Rho3 was greatly impaired, presumably due to mislocalization of these proteins in the sip1-i4 mutant cells. Furthermore, the interaction between Apm1 and Rho3 as well as Rho3 localization to the Golgi/endosomes were significantly rescued in sip1-i4 mutant cells by the expression of Sip1ΔN. Taken together, these results suggest that Sip1 recruits Rho3 to the Golgi/endosomes through physical interaction and enhances the formation of the Golgi/endosome AP-1/Rho3 complex, thereby promoting crosstalk between AP-1 and Rho3 in the regulation of Golgi/endosomal trafficking in fission yeast.

摘要

Rho 家族 GTPases 作为分子开关,调节多种生理功能,包括肌动蛋白细胞骨架的调节、膜运输、细胞形态、核基因表达和细胞生长。Rho 功能受其结合 GTP 的能力和定位调节。我们之前证明了 Rho3 与网格蛋白相关衔接蛋白-1(AP-1)复合物之间的功能和物理相互作用,这揭示了 Rho3 在调节裂殖酵母高尔基体/内体运输中的作用。Sip1 是一种保守的 AP-1 辅助蛋白,通过物理相互作用将 AP-1 复合物募集到高尔基体/内体。在这项研究中,我们表明 Sip1 是 Rho3 定位所必需的。首先,过量表达 rho3⁺ 可抑制 sip1-i4 突变细胞中与膜运输缺陷相关的缺陷,包括液泡融合、高尔基体/内体运输和分泌缺陷。值得注意的是,Sip1 与 Rho3 相互作用,与 Apm1-GFP 相似,GFP-Rho3 也不能在 27°C 时正确定位到 sip1-i4 突变细胞的高尔基体/内体。有趣的是,Sip1 的 C 端区域对于其定位于高尔基体/内体是必需的,因为 Sip1-i4-GFP 蛋白不能正确定位于高尔基体/内体,而 Sip1ΔN 突变蛋白的荧光与 FM4-64 的荧光共定位。一致地,在 sip1-i4 突变细胞中,缺乏 Sip1 的 C 端区域,Apm1 和 Rho3 之间的结合大大受损,可能是由于这些蛋白在 sip1-i4 突变细胞中的错误定位。此外,在 sip1-i4 突变细胞中,Sip1ΔN 的表达显著挽救了 Apm1 和 Rho3 之间的相互作用以及 Rho3 定位于高尔基体/内体。综上所述,这些结果表明,Sip1 通过物理相互作用将 Rho3 募集到高尔基体/内体,并增强高尔基体/内体 AP-1/Rho3 复合物的形成,从而促进裂殖酵母高尔基体/内体运输中 AP-1 和 Rho3 之间的串扰。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f3cb/3698097/c396a567ac3c/pone.0068488.g001.jpg

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