2003
DOI: 10.1128/ec.2.3.521-533.2003
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Novel Rho GTPase Involved in Cytokinesis and Cell Wall Integrity in the Fission Yeast Schizosaccharomyces pombe

Abstract: ؉ deletion or rho4 ؉ overexpression result in a defective cell wall, suggesting an additional role for Rho4 in cell wall integrity. rho4⌬ cells also accumulate secretory vesicles around the septum and are defective in actin polarization. We propose that Rho4 could be involved in the regulation of the septum degradation during cytokinesis.

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Cited by 59 publications
(89 citation statements)
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“…For example, our data showed that a general delay in cell separation caused by compromised functions of a wide range of proteins, including Ace2p, some of Ace2p's targets (Mid2p, Agn1p, and Eng1p), septins, exocyst component Sec8p, and small GTPase Rho4p, all allow SIN mutant cells to survive the stress imposed by a weak cell wall and septum (Table 3), probably because these mutations slow down or block the action of septum-degrading enzymes on the septum. In addition, we also found that the presence of sorbitol in the medium could rescue the cell lysis phenotype of some mutations in SIN pathway components ( Figure 3A), suggesting that SIN mutants might have septum defects, as sorbitol can act as an osmotic stabilizer and has been shown to rescue the cell lysis phenotype in mutants with a defective cell wall in both S. cerevisiae and S. pombe (Ribas et al 1991;Cid et al 1995;Santos et al 2003). Furthermore, overexpression of the Rho1p GTPase can also rescue the lysis phenotype of sid2-250.…”
Section: Discussionmentioning
confidence: 82%
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“…For example, our data showed that a general delay in cell separation caused by compromised functions of a wide range of proteins, including Ace2p, some of Ace2p's targets (Mid2p, Agn1p, and Eng1p), septins, exocyst component Sec8p, and small GTPase Rho4p, all allow SIN mutant cells to survive the stress imposed by a weak cell wall and septum (Table 3), probably because these mutations slow down or block the action of septum-degrading enzymes on the septum. In addition, we also found that the presence of sorbitol in the medium could rescue the cell lysis phenotype of some mutations in SIN pathway components ( Figure 3A), suggesting that SIN mutants might have septum defects, as sorbitol can act as an osmotic stabilizer and has been shown to rescue the cell lysis phenotype in mutants with a defective cell wall in both S. cerevisiae and S. pombe (Ribas et al 1991;Cid et al 1995;Santos et al 2003). Furthermore, overexpression of the Rho1p GTPase can also rescue the lysis phenotype of sid2-250.…”
Section: Discussionmentioning
confidence: 82%
“…One line of evidence came from our observation that the growth defect and the cell lysis defect can be rescued by addition of the sorbitol in the media ( Figure 3B). Sorbitol can act as an osmotic stabilizer and has been shown to rescue the cell lysis phenotype in mutants with a defective cell wall in both Saccharomyces cerevisiae and S. pombe (Ribas et al 1991;Cid et al 1995;Santos et al 2003). In addition, we also observed the phenotypic rescue of other mutations in SIN pathway components by the presence of sorbitol, such as sid4-A1, spg1-106, sid1-125, and mob1-1 (Figure 3B), suggesting that SIN mutants have septum defects that can be stabilized by sorbitol.…”
Section: Resultsmentioning
confidence: 99%
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“…By doing so, AnBud3, and by inference activated Rho4, may control additional steps beyond recruitment of SepA, such as maintenance of the CAR or coordination of septum deposition with ring constriction. (e.g., Nakano et al 2003;Santos et al 2003).…”
Section: Discussionmentioning
confidence: 99%
“…Given that there are four other Rho proteins (Rho2-Rho5) (Hirata et al, 1998;Nakano et al, 2002;Nakano et al, 2003;Santos et al, 2003;Wang et al, 2003) and several biochemically uncharacterized GEFs (Iwaki et al, 2003), it will take considerable effort in the future to sort out the biochemical specificities, cellular roles, and regulation of each Rho-GEF. In an effort to begin characterizing these proteins, Iwaki and colleagues deleted and overproduced the genes encoding all of them in fission yeast cells (Iwaki et al, 2003).…”
Section: Discussionmentioning
confidence: 99%