Wang Yue, Shaulsky Gad
Graduate Program in Structural Computational Biology and Molecular Biophysics, Baylor College of Medicine, Houston, Texas, 77030, United States of America.
Graduate Program in Structural Computational Biology and Molecular Biophysics, Baylor College of Medicine, Houston, Texas, 77030, United States of America; Department of Molecular and Human Genetics, Baylor College of Medicine, Houston Texas, 77030, United States of America.
PLoS One. 2015 Apr 20;10(4):e0124270. doi: 10.1371/journal.pone.0124270. eCollection 2015.
The cell adhesion glycoproteins, TgrB1 and TgrC1, are essential for Dictyostelium development and allorecognition, but it has been impossible to determine whether their pleiotropic roles are due to one common function or to distinct functions in separate pathways. Mutations in the respective genes, tgrB1 and tgrC1, abrogate both development and allorecognition and the defects cannot be suppressed by activation of the cyclic AMP dependent protein kinase PKA, a central regulator of Dictyostelium development. Here we report that mutations in genes outside the known PKA pathway partially suppress the tgrC1-null developmental defect. We separated the pleiotropic roles of tgrC1 by testing the effects of a suppression mutation, stcinsA under different conditions. stcAins modified only the developmental defect of tgrC1- but not the allorecognition defect, suggesting that the two functions are separable. The suppressor mutant phenotype also revealed that tgrC1 regulates stalk differentiation in a cell-autonomous manner and spore differentiation in a non-cell-autonomous manner. Moreover, stcAins did not modify the developmental defect of tgrB1-, but the less robust phenotype of tgrB1- obscures the possible role of stcA relative to tgrB1.
细胞黏附糖蛋白TgrB1和TgrC1对盘基网柄菌的发育和同种异体识别至关重要,但一直无法确定它们的多效性作用是由于一种共同功能还是在不同途径中的不同功能。tgrB1和tgrC1各自基因的突变会消除发育和同种异体识别,并且这些缺陷不能通过激活环磷酸腺苷依赖性蛋白激酶PKA(盘基网柄菌发育的核心调节因子)来抑制。在此我们报告,已知PKA途径之外的基因中的突变部分抑制了tgrC1基因缺失导致的发育缺陷。我们通过测试抑制突变stcAins在不同条件下的作用来区分tgrC1的多效性作用。stcAins仅改变了tgrC1的发育缺陷,而没有改变同种异体识别缺陷,这表明这两种功能是可分离的。抑制突变体表型还表明,tgrC1以细胞自主方式调节柄细胞分化,以非细胞自主方式调节孢子分化。此外,stcAins没有改变tgrB1的发育缺陷,但tgrB1较弱的表型掩盖了stcA相对于tgrB1可能的作用。