Page B D, Guedes S, Waring D, Priess J R
Division of Basic Sciences, Fred Hutchinson Cancer Research Center, Seattle, Washington 98109, USA.
Mol Cell. 2001 Mar;7(3):451-60. doi: 10.1016/s1097-2765(01)00193-9.
Early C. elegans embryos exhibit protein asymmetries that allow rapid diversification of cells. Establishing these asymmetries requires the novel protein MEX-5. We show that mutations in the efl-1 and dpl-1 genes cause defects in protein localization resembling defects caused by mutations in mex-5. efl-1 and dpl-1 encode homologs of vertebrate E2F and DP proteins that regulate transcription as a heterodimer. efl-1 and dpl-1 mutants have elevated levels of activated Map kinase in oocytes. Their mutant phenotype and that of mex-5 mutants can be suppressed by reducing Ras/Map kinase signaling. We propose this signaling pathway has a role in embryonic asymmetry and that EFL-1/DPL-1 control the level of Map kinase activation.
早期秀丽隐杆线虫胚胎表现出蛋白质不对称性，这使得细胞能够快速分化。建立这些不对称性需要新的蛋白质MEX-5。我们发现，efl-1和dpl-1基因的突变会导致蛋白质定位缺陷，类似于mex-5基因突变所导致的缺陷。efl-1和dpl-1编码脊椎动物E2F和DP蛋白的同源物，它们作为异二聚体调节转录。efl-1和dpl-1突变体的卵母细胞中活化的丝裂原活化蛋白激酶（Map激酶）水平升高。通过降低Ras/Map激酶信号传导，可以抑制它们的突变表型以及mex-5突变体的表型。我们提出，该信号通路在胚胎不对称性中起作用，并且EFL-1/DPL-1控制Map激酶的活化水平。
