详细信息
Sro7 and Sro77, the yeast homologues of the Drosophila lethal giant larvae (Lgl), regulate cell proliferation via the Rho1-Tor1 pathway ( SCI-EXPANDED收录)
文献类型:期刊文献
英文题名:Sro7 and Sro77, the yeast homologues of the Drosophila lethal giant larvae (Lgl), regulate cell proliferation via the Rho1-Tor1 pathway
作者:Liou, Liang-Chun[1];Ren, Qun[1];Gao, Qiuqiang[2];Zhang, Zhaojie[1]
机构:[1]Univ Wyoming, Dept Zool & Physiol, Laramie, WY 82071 USA;[2]E China Univ Sci & Technol, State Key Lab Bioreactor Engn, Shanghai 200237, Peoples R China
年份:2014
卷号:160
起止页码:2208
外文期刊名:MICROBIOLOGY-SGM
收录:;WOS:【SCI-EXPANDED(收录号:WOS:000345495700010)】;
基金:This study was supported in part by an Institutional Development Award from the National Institute of General Medical Sciences of the National Institutes of Health (grant P30 GM103398).
语种:英文
摘要:Saccharomyces cerevisiae Sro7 and Sro77 are homologues of the Drosophila tumour suppressor lethal giant larvae (Lgl), which regulates cell polarity in Drosophila epithelial cells. Here, we showed that double mutation of SRO7/SRO77 was defective in colony growth. The colony of the SRO7/SRO77 double deletion was much smaller than the WT and appeared to be round with a smooth surface, compared with the WT. Analysis using transmission electron microscopy revealed multiple defects of the colony cells, including multiple budding, multiple nuclei, cell lysis and dead cells, suggesting that the double deletion caused defects in cell polarity and cell wall integrity (CWI). Overexpression of RHO1, one of the central regulators of cell polarity and CWI, fully recovered the sro7 Delta/sro77 Delta, phenotype. We further demonstrated that sro7 Delta/sro77 Delta caused a decrease of the GTP-bound, active Rho1, which in turn caused an upregulation of TOR1. Deletion of TOR1 in sro7 Delta/sro77 Delta (sro7 Delta/sro77 Delta/tor1 Delta) recovered the cell growth and colony morphology, similar to WT. Our results suggested that the tumour suppressor homologue SRO7/SRO77 regulated cell proliferation and yeast colony development via the Rho1-Tor1 pathway.
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