Roles of Hof1p, Bni1p, Bnr1p, and Myo1p in Cytokinesis inSaccharomyces cerevisiae

Abstract

Cytokinesis in Saccharomyces cerevisiae occurs by the concerted action of the actomyosin system and septum formation. Here we report on the roles of HOF1, BNI1, and BNR1 in cytokinesis, focusing on Hof1p. Deletion of HOF1 causes a temperature-sensitive defect in septum formation. A Hof1p ring forms on the mother side of the bud neck in G2/M, followed by the formation of a daughter-side ring. Around telophase, Hof1p is phosphorylated and the double rings merge into a single ring that contracts slightly and may colocalize with the actomyosin structure. Upon septum formation, Hof1p splits into two rings, disappearing upon cell separation. Hof1p localization is dependent on septins but not Myo1p. Synthetic lethality suggests that Bni1p and Myo1p belong to one functional pathway, whereas Hof1p and Bnr1p belong to another. These results suggest that Hof1p may function as an adapter linking the primary septum synthesis machinery to the actomyosin system. The formation of the actomyosin ring is not affected by bni1Delta, hof1Delta, or bnr1Delta. However, Myo1p contraction is affected by bni1Delta but not by hof1Delta or bnr1Delta. In bni1Delta cells that lack the actomyosin contraction, septum formation is often slow and asymmetric, suggesting that actomyosin contraction may provide directionality for efficient septum formation.

Stable and Dynamic Axes of Polarity Use Distinct Formin Isoforms in Budding Yeast

“…However, strains lacking Bnr1p still transport vesicles from the mother to concentrate at the bud tip ( Figure 3A) and are able to grow with a normal morphology and rate (Imamura et al, 1997;Vallen et al, 2000), suggesting that the few Bni1p-dependent cables in the mother cell meet the transport requirements of the yeast cell under the conditions examined so far.…”

“…Both formins promote actin cable assembly Sagot et al, 2002a), but the loss of Bnr1p causes only a mild delay in cell separation (Vallen et al, 2000), whereas the absence of Bni1p causes a widened bud neck (Jansen et al, 1996;Zahner et al, 1996;Mosch and Fink, 1997;Sheu et al, 2000), an inability to engage in tip-directed growth (Evangelista et al, 1997;Mosch and Fink, 1997;Sheu et al, 2000;Ozaki-Kuroda et al, 2001), a defect in bipolar bud site selection (Zahner et al, 1996), a partial defect in cytokinetic ring contraction (Vallen et al, 2000), a defect in early spindle alignment Lee et al, 1999), and a variety of synthetic lethal genetic interactions (Kohno et al, 1996;Longtine et al, 1996;Fujiwara et al, 1998;Fujiwara et al, 1999;Lee et al, 1999;Tong et al, 2001Tong et al, , 2004. We suggest that many, if not all, of these can be attributed to the actin assembly activity of the two formins in conjunction with their specific localizations.…”

“…Both formins support the assembly of the contractile ring (Vallen et al, 2000), so we did not examine that structure. Cables in bnr1⌬/ bnr1⌬ cells were similar to wild-type yeast, but they were more likely to be disorganized in bni1⌬/bni1⌬ cells (Figure 1, C and D).…”

Dosage rescue by UBC4 restores cell wall integrity in Saccharomyces cerevisiae lacking the myosin type II gene MYO1

“…In anticipation that interactions might already be described between myo1 and/or chs3 mutations and genes identified by our screen, we searched in the Saccharomyces cerevisiae Genome Database (SGD) (http://www.yeastgenome.org/). We found that a total of 10 synthetic lethal interactions (Breton and Aigle, 1998;Davierwala et al, 2005;Roumanie et al, 2000;Vallen et al, 2000;Wang and Bretscher, 1995) and two synthetic growth interactions (Lillie and Brown, 1998) have been previously described for myo1, while 76 synthetic lethal (Friesen et al, 2006;Goehring et al, 2003;Lesage et al, 2005;Tong et al, 2004) and two synthetic growth interactions (Castrejon et al, 2006;Sobering et al, 2004) have been previously described for chs3. There were no common synthetic lethal or synthetic growth interactions described between myo1 and chs3 in the SGD, although we and others have reported a synthetic growth interaction (Rivera-Molina et al, 2006;Schmidt et al, 2002).…”

“…Absence of the actomyosin ring in yeast caused by a deletion of the MYO1 gene activates a functionally redundant cytokinesis pathway, regulated by a cytoskeletal binding protein Hof1p (Korinek et al, 2000;Vallen et al, 2000). This mechanism requires increased deposition of chitin at the bud neck by chitin synthase III (CSIII) (Schmidt et al, 2002;Tolliday et al, 2003).…”