Lte1 contributes to Bfa1 localization rather than stimulating nucleotide exchange by Tem1

Geymonat, Marco; Spanos, Adonis; Bettignies, Geoffroy de; Sedgwick, Steven G.

doi:10.1083/jcb.200905114

Cited by 61 publications

(102 citation statements)

References 63 publications

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“…Under this hypothesis, Etd1 might antagonize PP2A-Pab1 function through Spg1 GAP(s) inactivation and delocalization rather than by GEF activity stimulating Spg1 nucleotide exchange. In agreement with this possibility, Lte1 has been shown to activate Tem1 by regulating the localization of the GAP Bfa1 at the SPBs (Geymonat et al 2009). …”

Section: Resultsmentioning

confidence: 62%

Antagonistic Roles of PP2A-Pab1 and Etd1 in the Control of Cytokinesis in Fission Yeast

et al. 2010

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In Schizosaccharomyces pombe, Etd1 is a positive regulator of the septation initiation network (SIN), a conserved GTPase-regulated kinase cascade that triggers cytokinesis. Here we show that a mutation in the pab1 gene, which encodes the B-regulatory subunit of the protein phosphatase 2A (PP2A), suppresses mutations in the etd1 gene. Etd1 is required for the function of the GTPase Spg1, a key regulator of SIN signaling. Interestingly, the loss of Pab1 function restored the activity of Spg1 in Etd1-deficient cells. This result suggests that PP2A-Pab1-mediated dephosphorylation inhibits Spg1, thus antagonizing Etd1 function. The loss of pab1 function also rescues the lethality of mutants of other genes in the SIN cascade such as mob1, sid1, and cdc11. Two-hybrid assays indicate that Pab1 physically interacts with Mob1, Sid1, Sid2, and Cdc11, suggesting that the phosphatase 2A B-subunit is a component of the SIN complex. Together, our results indicate that PP2A-Pab1 plays a novel role in cytokinesis, regulating SIN activity at different levels. Pab1 is also required to activate polarized cell growth. Thus, PP2A-Pab1 may be involved in coordinating polar growth and cytokinesis.

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Section: Resultsmentioning

confidence: 62%

Antagonistic Roles of PP2A-Pab1 and Etd1 in the Control of Cytokinesis in Fission Yeast

et al. 2010

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“…Lte1 localizes to the bud cortex (Figure 12), leading to early models in which SPB migration into the daughter cell directly promotes GTP loading on Tem1. Recent studies suggest that Lte1 does not serve this purpose; rather, it appears to block the function of the protein kinase Kin4, which as discussed further below is an inhibitor of the MEN (Geymonat et al 2009;Chan and Amon 2010;Bertazzi et al 2011). Overall, the mechanism by which Lte1 activates the MEN remains uncertain.…”

Section: Menmentioning

confidence: 99%

“…Regardless, assembly and function of the Bub2-Bfa1 complex is clearly a key aspect of MEN regulation (Fraschini et al 2006;Geymonat et al 2009). Like other MEN components, Bub2-Bfa1 localizes to the SPB, with a notable bias to the pole that migrates into the daughter cell cytoplasm; in fact, the complex strongly stabilizes SBP localization of Tem1 (Bardin et At least two distinct models have been proposed for Bub2-Bfa1's control of mitotic exit.…”

Section: Menmentioning

confidence: 99%

Mitotic Exit and Separation of Mother and Daughter Cells

2012

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Productive cell proliferation involves efficient and accurate splitting of the dividing cell into two separate entities. This orderly process reflects coordination of diverse cytological events by regulatory systems that drive the cell from mitosis into G1. In the budding yeast Saccharomyces cerevisiae, separation of mother and daughter cells involves coordinated actomyosin ring contraction and septum synthesis, followed by septum destruction. These events occur in precise and rapid sequence once chromosomes are segregated and are linked with spindle organization and mitotic progress by intricate cell cycle control machinery. Additionally, critical parts of the mother/daughter separation process are asymmetric, reflecting a form of fate specification that occurs in every cell division. This chapter describes central events of budding yeast cell separation, as well as the control pathways that integrate them and link them with the cell cycle.

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“…The protein is essential for exit from mitosis at low temperatures and has homology to guanine nucleotide exchange factors (GEFs). Despite this homology, Lte1 GEF activity has, however, not been detected in vitro (16,17). Here, prompted by the observation that when Kin4 and Lte1 reside in the same compartment, Lte1 activation of the MEN prevails over Kin4 inhibition (4,(17)(18)(19), we investigate the possibility that Lte1 inhibits Kin4.…”

mentioning

confidence: 99%

Lte1 promotes mitotic exit by controlling the localization of the spindle position checkpoint kinase Kin4

Falk

Chan

Amon

2011

Proc. Natl. Acad. Sci. U.S.A.

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For a daughter cell to receive a complete genomic complement, it is essential that the mitotic spindle be positioned accurately within the cell. In budding yeast, a signaling system known as the spindle position checkpoint (SPOC) monitors spindle position and regulates the activity of the mitotic exit network (MEN), a GTPase signaling pathway that promotes exit from mitosis. The protein kinase Kin4 is a central component of the spindle position checkpoint. Kin4 primarily localizes to the mother cell and associates with spindle pole bodies (SPBs) located in the mother cell to inhibit MEN signaling. In contrast, the kinase does not associate with the SPB in the bud. Thus, only when a MEN bearing SPB leaves the mother cell and the spindle is accurately positioned along the mother–bud axis can MEN signaling occur and cell division proceed. Here, we describe a mechanism ensuring that Kin4 only associates with mother cell-located SPBs. The bud-localized MEN regulator Lte1, whose molecular function has long been unclear, prevents Kin4 that escapes into the bud from associating with SPBs in the daughter cell.

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Lte1 contributes to Bfa1 localization rather than stimulating nucleotide exchange by Tem1

Abstract: Reevaluation of Lte1’s involvement in the mitotic exit network reveals that it is involved in localizing Bfa1 to the spindle pole body but does not function as a GEF for Tem1.

Cited by 61 publications

References 63 publications

Antagonistic Roles of PP2A-Pab1 and Etd1 in the Control of Cytokinesis in Fission Yeast

Antagonistic Roles of PP2A-Pab1 and Etd1 in the Control of Cytokinesis in Fission Yeast

Mitotic Exit and Separation of Mother and Daughter Cells

Lte1 promotes mitotic exit by controlling the localization of the spindle position checkpoint kinase Kin4

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