G protein α subunit suppresses sporangium formation through a serine/threonine protein kinase in Phytophthora sojae.,PLoS Pathogens

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G protein α subunit suppresses sporangium formation through a serine/threonine protein kinase in Phytophthora sojae.
PLoS Pathogens ( IF 5.5 ) Pub Date : 2020-01-21 , DOI: 10.1371/journal.ppat.1008138
Min Qiu _{1,

2} , Yaning Li _{1,

2} , Xin Zhang _{1,

2} , Mingrun Xuan _{1,

2} , Baiyu Zhang _{1,

2} , Wenwu Ye _{1,

2} , Xiaobo Zheng _{1,

2} , Francine Govers ₃ , Yuanchao Wang _{1,

2}

Affiliation

Eukaryotic heterotrimeric guanine nucleotide-binding proteins consist of α, β, and γ subunits, which act as molecular switches to regulate a number of fundamental cellular processes. In the oomycete pathogen Phytophthora sojae, the sole G protein α subunit (Gα; encoded by PsGPA1) has been found to be involved in zoospore mobility and virulence, but how it functions remains unclear. In this study, we show that the Gα subunit PsGPA1 directly interacts with PsYPK1, a serine/threonine protein kinase that consists of an N-terminal region with unknown function and a C-terminal region with a conserved catalytic kinase domain. We generated knockout and knockout-complemented strains of PsYPK1 and found that deletion of PsYPK1 resulted in a pronounced reduction in the production of sporangia and oospores, in mycelial growth on nutrient poor medium, and in virulence. PsYPK1 exhibits a cytoplasmic-nuclear localization pattern that is essential for sporangium formation and virulence of P. sojae. Interestingly, PsGPA1 overexpression was found to prevent nuclear localization of PsYPK1 by exclusively binding to the N-terminal region of PsYPK1, therefore accounting for its negative role in sporangium formation. Our data demonstrate that PsGPA1 negatively regulates sporangium formation by repressing the nuclear localization of its downstream kinase PsYPK1.

中文翻译：

G 蛋白 α 亚基通过酱油疫霉中的丝氨酸/苏氨酸蛋白激酶抑制孢子囊形成。

真核异三聚鸟嘌呤核苷酸结合蛋白由 α、β 和 γ 亚基组成，它们充当调节许多基本细胞过程的分子开关。在卵菌病原体酱油疫霉中，唯一的 G 蛋白 α 亚基（Gα；由 PsGPA1 编码）已被发现与游动孢子的活动性和毒力有关，但其功能如何仍不清楚。在这项研究中，我们发现 Gα 亚基 PsGPA1 直接与 PsYPK1 相互作用，PsYPK1 是一种丝氨酸/苏氨酸蛋白激酶，由功能未知的 N 端区域和具有保守催化激酶结构域的 C 端区域组成。我们生成了 PsYPK1 敲除菌株和敲除互补菌株，发现 PsYPK1 敲除会导致孢子囊和卵孢子的产生、营养不良培养基上菌丝体的生长以及毒力显着减少。 PsYPK1 表现出细胞质-核定位模式，这对于酱油青霉的孢子囊形成和毒力至关重要。有趣的是，PsGPA1 过表达被发现通过专门结合 PsYPK1 的 N 末端区域来阻止 PsYPK1 的核定位，因此解释了其在孢子囊形成中的负面作用。我们的数据表明，PsGPA1 通过抑制其下游激酶 PsYPK1 的核定位来负向调节孢子囊形成。

更新日期：2020-01-22

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