Department of Microbiology and Molecular Genetics, Oklahoma State University, Stillwater, OK 74078-3020, USA.
Microbiology (Reading). 2010 Mar;156(Pt 3):789-797. doi: 10.1099/mic.0.036541-0. Epub 2009 Dec 17.
The Dictyostelium Galpha5 subunit has been shown to reduce cell viability, inhibit folate chemotaxis and accelerate tip morphogenesis and gene expression during multicellular development. Alteration of the D-motif (mitogen-activated protein kinase docking site) at the amino terminus of the Galpha 5 subunit or the loss of extracellular signal-regulated kinase (ERK)1 diminished the lethality associated with the overexpression or constitutive activation of the Galpha5 subunit. The amino-terminal D-motif of the Galpha5 subunit was also found to be necessary for the reduced cell size, small aggregate formation and precocious developmental gene expression associated with Galpha5 subunit overexpression. This D-motif also contributed to the aggregation delay in cells expressing a constitutively active Galpha5 subunit, but the D-motif was not necessary for the inhibition of folate chemotaxis. These results suggest that the amino-terminal D-motif is required for some but not all phenotypes associated with elevated Galpha5 subunit functions during growth and development and that ERK1 can function in Galpha5 subunit-mediated signal transduction.
已证实，Dictyostelium 中的 Galpha5 亚基可降低细胞活力、抑制叶酸趋化性，并在细胞的多细胞发育过程中加速尖端形态发生和基因表达。改变 Galpha5 亚基氨基末端的 D 基序（有丝分裂原激活蛋白激酶 docking 位点）或缺失细胞外信号调节激酶（ERK）1，可减少 Galpha5 亚基过表达或组成性激活相关的致死性。还发现，Galpha5 亚基的氨基末端 D 基序对于与 Galpha5 亚基过表达相关的细胞体积减小、小聚集体形成和早期发育基因表达也是必需的。该 D 基序还可导致表达组成性激活的 Galpha5 亚基的细胞的聚集延迟，但对于叶酸趋化性的抑制则不是必需的。这些结果表明，氨基末端 D 基序对于生长和发育过程中 Galpha5 亚基功能升高相关的某些表型是必需的，但对于 Galpha5 亚基介导的信号转导，ERK1 可发挥作用。
