PKC1, a protein kinase C homologue of Saccharomyces cerevisiae, participates in microtubule function through the yeast EB1 homologue, BIM1

Hosotani, Tomoki; Koyama, Hirofumi; Uchino, Masayuki; Miyakawa, Tokichi; Tsuchiya, Eiko

doi:10.1046/j.1365-2443.2001.00461.x

Cited by 24 publications

(29 citation statements)

References 40 publications

(57 reference statements)

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“…PKCs have been associated with MTs in many cell types (Kiley and Parker, 1995;Garcia-Rocha et al, 1997;Hosotani et al, 2001;Kabir et al, 2001;Szalay et al, 2001;Nakhost et al, 2002), and, in yeast, PKC1 regulates the function of MTs through BIM1, the yeast EB1 homologue (Hosotani et al, 2001). As shown in this study, however, PKC inhibition by Gö-6976 had no effect on the recruitment of EB1 upon cell membrane disruption.…”

Section: Discussionmentioning

confidence: 40%

Disruption of the plasma membrane stimulates rearrangement of microtubules and lipid traffic toward the wound site

Togo¹

2006

Journal of Cell Science

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Resealing of a disrupted plasma membrane requires Ca2+-regulated exocytosis. Repeated disruptions reseal more quickly than the initial wound. This facilitated response requires both Ca2+ and protein kinase C (PKC), and is sensitive to brefeldin A. There is also evidence that this response is polarized to the site where the cell membrane had previously been disrupted. Observations of GFP-tagged α-tubulin and end-binding protein 1 (EB1) revealed that membrane disruption initially induced disassembly of microtubules around the wound site, followed by elongation of microtubules toward the wound site. Recruitment of EB1 to microtubules required Ca2+ influx, but was independent of PKC. NBD C6-ceramide, a probe for the Golgi apparatus and Golgi-derived lipids, initially stained the perinuclear region, and a portion of the probe was translocated to the wound site 5 minutes after wounding. Translocation of the lipids required microtubules and PKC activity, and was suppressed by low temperature. On the other hand, constitutive traffic of the lipid was still normal in the presence of a PKC inhibitor. These findings suggest that membrane disruption stimulates regulated vesicle traffic from the region of the trans-Golgi network to the wound site along rearranged microtubules in a PKC-dependent manner.

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Section: Discussionmentioning

confidence: 40%

Disruption of the plasma membrane stimulates rearrangement of microtubules and lipid traffic toward the wound site

Togo¹

2006

Journal of Cell Science

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“…A rom2⌬ mutant and a pkc1(Ts) mutant but not an mpk1⌬ mutant were found to be hypersensitive to the microtubule antagonists benomyl and thiabendazole, respectively (124,201). Conversely, overexpression of Pkc1 confers thiabendazole resistance on wildtype cells (124). Interestingly, these authors also demonstrated that a pkc1(Ts) mutant displays a G 2 delay and aberrant nuclear positioning in a fraction of the cells at semipermissive temperature, supporting the notion that Pkc1 plays a role in microtubule or SPB function.…”

Section: Nuclear Functions Of Pkc1mentioning

confidence: 99%

Section: Nuclear Functions Of Pkc1mentioning

confidence: 99%

Cell Wall Integrity Signaling inSaccharomyces cerevisiae

Levin¹

2005

Microbiol Mol Biol Rev

1,048

1,227

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The yeast cell wall is a highly dynamic structure that is responsible for protecting the cell from rapid changes in external osmotic potential. The wall is also critical for cell expansion during growth and morphogenesis. This review discusses recent advances in understanding the various signal transduction pathways that allow cells to monitor the state of the cell wall and respond to environmental challenges to this structure. The cell wall integrity signaling pathway controlled by the small G-protein Rho1 is principally responsible for orchestrating changes to the cell wall periodically through the cell cycle and in response to various forms of cell wall stress. This signaling pathway acts through direct control of wall biosynthetic enzymes, transcriptional regulation of cell wall-related genes, and polarization of the actin cytoskeleton. However, additional signaling pathways interface both with the cell wall integrity signaling pathway and with the actin cytoskeleton to coordinate polarized secretion with cell wall expansion. These include Ca2+ signaling, phosphatidylinositide signaling at the plasma membrane, sphingoid base signaling through the Pkh1 and -2 protein kinases, Tor kinase signaling, and pathways controlled by the Rho3, Rho4, and Cdc42 G-proteins

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“…First, conditional pkc1 mutants undergo cell lysis uniformly with small buds and duplicated DNA, but prior to spindle pole body (SPB) separation (Levin et al 1990;Levin and Bartlett-Heubusch 1992). Second, under growth conditions in which cell lysis was prevented by osmotic support, a conditional pkc1 mutant was shown to linger at G 2 /M, a phenotype that was attributed to a delay in spindle elongation (Hosotani et al 2001). Third, several studies have revealed genetic connections between Pkc1 and the chromatin remodeling complex called RSC (reviewed in Levin 2005), which serves a critical function in the progression from G 2 to mitosis.…”

Section: Rho1 Activation During Cytokinesismentioning

confidence: 99%

Regulation of Cell Wall Biogenesis in Saccharomyces cerevisiae: The Cell Wall Integrity Signaling Pathway

2011

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The yeast cell wall is a strong, but elastic, structure that is essential not only for the maintenance of cell shape and integrity, but also for progression through the cell cycle. During growth and morphogenesis, and in response to environmental challenges, the cell wall is remodeled in a highly regulated and polarized manner, a process that is principally under the control of the cell wall integrity (CWI) signaling pathway. This pathway transmits wall stress signals from the cell surface to the Rho1 GTPase, which mobilizes a physiologic response through a variety of effectors. Activation of CWI signaling regulates the production of various carbohydrate polymers of the cell wall, as well as their polarized delivery to the site of cell wall remodeling. This review article centers on CWI signaling in Saccharomyces cerevisiae through the cell cycle and in response to cell wall stress. The interface of this signaling pathway with other pathways that contribute to the maintenance of cell wall integrity is also discussed.

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PKC1, a protein kinase C homologue of Saccharomyces cerevisiae, participates in microtubule function through the yeast EB1 homologue, BIM1

Abstract: Background: RSC is a chromatin-remodelling complex of Saccharomyces cerevisiae and essential for growth. Its catalytic subunit is encoded by the NPS1/STH1 gene. At the present time, little is known regarding the cellular function of RSC.

Cited by 24 publications

References 40 publications

Disruption of the plasma membrane stimulates rearrangement of microtubules and lipid traffic toward the wound site

Disruption of the plasma membrane stimulates rearrangement of microtubules and lipid traffic toward the wound site

Cell Wall Integrity Signaling inSaccharomyces cerevisiae

Regulation of Cell Wall Biogenesis in Saccharomyces cerevisiae: The Cell Wall Integrity Signaling Pathway

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