Open AccessSro7 and Sro77, the yeast homologues of the Drosophila lethal giant larvae (Lgl), regulate cell proliferation via the Rho1–Tor1 pathway
Author(s) -
Liang-Chun Liou,
Qun Ren,
Qinghai Gao,
Zhaojie Zhang
Publication year - 2014
Publication title -
microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.019
H-Index - 179
eISSN - 1465-2080
pISSN - 1350-0872
DOI - 10.1099/mic.0.080234-0
Subject(s) - biology , cell growth , microbiology and biotechnology , phenotype , budding , yeast , saccharomyces cerevisiae , cell , cell cycle , cell polarity , downregulation and upregulation , mutation , budding yeast , genetics , gene
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 Δ/ sro77 Δ phenotype. We further demonstrated that sro7 Δ/ sro77 Δ caused a decrease of the GTP-bound, active Rho1, which in turn caused an upregulation of TOR1 . Deletion of TOR1 in sro7 Δ/ sro77 Δ ( sro7 Δ/ sro77 Δ/ tor1 Δ) 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.