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首页> 外文期刊>Eukaryotic cell >Role of Phosphatidylinositol Phosphate Signaling in the Regulation of the Filamentous-Growth Mitogen-Activated Protein Kinase Pathway
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Role of Phosphatidylinositol Phosphate Signaling in the Regulation of the Filamentous-Growth Mitogen-Activated Protein Kinase Pathway

机译：磷脂酰肌醇磷酸信号在丝状生长丝裂原活化蛋白激酶途径调控中的作用

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Reversible phosphorylation of the phospholipid phosphatidylinositol (PI) is a key event in the determination of organelle identity and an underlying regulatory feature in many biological processes. Here, we investigated the role of PI signaling in the regulation of the mitogen-activated protein kinase (MAPK) pathway that controls filamentous growth in yeast. Lipid kinases that generate phosphatidylinositol 4-phosphate [PI(4)P] at the Golgi (Pik1p) or PI(4,5)P2 at the plasma membrane (PM) (Mss4p and Stt4p) were required for filamentous-growth MAPK pathway signaling. Introduction of a conditional allele of PIK1 (pik1-83) into the filamentous (Σ1278b) background reduced MAPK activity and caused defects in invasive growth and biofilm/mat formation. MAPK regulatory proteins that function at the PM, including Msb2p, Sho1p, and Cdc42p, were mislocalized in the pik1-83 mutant, which may account for the signaling defects of the PI(4)P kinase mutants. Other PI kinases (Fab1p and Vps34p), and combinations of PIP (synaptojanin-type) phosphatases, also influenced the filamentous-growth MAPK pathway. Loss of these proteins caused defects in cell polarity, which may underlie the MAPK signaling defect seen in these mutants. In line with this possibility, disruption of the actin cytoskeleton by latrunculin A (LatA) dampened the filamentous-growth pathway. Various PIP signaling mutants were also defective for axial budding in haploid cells, cell wall construction, or proper regulation of the high-osmolarity glycerol response (HOG) pathway. Altogether, the study extends the roles of PI signaling to a differentiation MAPK pathway and other cellular processes.
机译：磷脂磷脂酰肌醇（PI）的可逆磷酸化是确定细胞器身份和许多生物学过程中潜在的调控特征的关键事件。在这里，我们研究了PI信号传导在控制酵母丝状生长的丝裂原活化蛋白激酶（MAPK）途径调控中的作用。丝状生长MAPK途径信号需要在高尔基体（Pik1p）产生磷脂酰磷酸4磷酸[PI（4）P]或质膜（PM）（Mss4p和Stt4p）产生PI（4,5）P2的脂质激酶。 。在丝状（Σ1278b）背景中引入 PIK1 （ pik1-83 ）有条件等位基因会降低MAPK活性，并导致侵袭性生长和生物膜/垫形成的缺陷。在PM处起作用的MAPK调节蛋白（包括Msb2p，Sho1p和Cdc42p）在 pik1-83 突变体中错位，这可能是PI（4）P激酶突变体的信号缺陷的原因。其他PI激酶（Fab1p和Vps34p）以及PIP（突触核蛋白型）磷酸酶的组合也影响了丝状生长MAPK途径。这些蛋白质的丢失导致细胞极性缺陷，这可能是这些突变体中见到的MAPK信号缺陷的基础。与这种可能性相一致的是，latrunculin A（LatA）对肌动蛋白细胞骨架的破坏抑制了丝状生长途径。各种PIP信号突变体在单倍体细胞中的轴向萌芽，细胞壁结构或高渗甘油反应（HOG）途径的适当调节方面也存在缺陷。总之，这项研究将PI信号传导的作用扩展到了分化MAPK途径和其他细胞过程。

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