Latrunculin A Delays Anaphase Onset in Fission Yeast by Disrupting an Ase1-independent Pathway Controlling Mitotic Spindle Stability

Meadows, John C.; Millar, Jonathan

doi:10.1091/mbc.e08-02-0164

Cited by 21 publications

(15 citation statements)

References 73 publications

(86 reference statements)

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“…permissive temperature ( Figure 3A); the cohesin mutant pcs3-T1 (Nonaka et al, 2002;Kawashima et al, 2007; Figure 3B); and the dam1⌬ mutant ( Figure 3C), which impairs the function of the DASH complex in kinetochore-microtubule attachment (Sanchez-Perez et al, 2005). In all three mutants, lack of Bub3p caused no impairment in spindle checkpointdependent delay/arrest, consistent with other recent studies (Meadows and Millar, 2008;Tange and Niwa, 2008;Windecker et al, 2009), but resulted in a dramatic loss of viability. Moreover, our data suggest that lack of Bub3 accentuates the cell cycle delay in response to these spindle attachment defects(see below).…”

Section: Loss Of Bub3p Accentuates the Cell Cycle Delay In Response Tsupporting

confidence: 85%

Bub3p Facilitates Spindle Checkpoint Silencing in Fission Yeast

Vanoosthuyse

Meadows

Sar

et al. 2009

MBoC

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Although critical for spindle checkpoint signaling, the role kinetochores play in anaphase promoting complex (APC) inhibition remains unclear. Here we show that spindle checkpoint proteins are severely depleted from unattached kinetochores in fission yeast cells lacking Bub3p. Surprisingly, a robust mitotic arrest is maintained in the majority of bub3 Delta cells, yet they die, suggesting that Bub3p is essential for successful checkpoint recovery. During recovery, two defects are observed: (1) cells mis-segregate chromosomes and (2) anaphase onset is significantly delayed. We show that Bub3p is required to activate the APC upon inhibition of Aurora kinase activity in checkpoint-arrested cells, suggesting that Bub3p is required for efficient checkpoint silencing downstream of Aurora kinase. Together, these results suggest that spindle checkpoint signals can be amplified in the nucleoplasm, yet kinetochore localization of spindle checkpoint components is required for proper recovery from a spindle checkpoint-dependent arrest.

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Section: Loss Of Bub3p Accentuates the Cell Cycle Delay In Response Tsupporting

confidence: 85%

Bub3p Facilitates Spindle Checkpoint Silencing in Fission Yeast

Vanoosthuyse

Meadows

Sar

et al. 2009

MBoC

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“…Sty1 is the fission yeast homolog of budding yeast MAP kinase Hog1 and of mammalian stress-activated protein kinase (SAPK) p38 [18, 19, 20]. Although there is now considerable evidence against the concept of a spindle orientation checkpoint [21, 22, 23], the initial observation of Sty1 activation after latrunculin B treatment was never investigated further. We therefore decided to revisit the question of how the Cdc42 polarity module disperses from cell tips after LatA treatment, and whether Sty1 plays a role in this behavior.…”

Section: Resultsmentioning

confidence: 99%

Remodeling of the Fission Yeast Cdc42 Cell-Polarity Module via the Sty1 p38 Stress-Activated Protein Kinase Pathway

2016

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SummaryThe Rho family GTPase Cdc42 is a key regulator of eukaryotic cellular organization and cell polarity [1]. In the fission yeast Schizosaccharomyces pombe, active Cdc42 and associated effectors and regulators (the “Cdc42 polarity module”) coordinate polarized growth at cell tips by controlling the actin cytoskeleton and exocytosis [2, 3, 4]. Localization of the Cdc42 polarity module to cell tips is thus critical for its function. Here we show that the fission yeast stress-activated protein kinase Sty1, a homolog of mammalian p38 MAP kinase, regulates localization of the Cdc42 polarity module. In wild-type cells, treatment with latrunculin A, a drug that leads to actin depolymerization, induces dispersal of the Cdc42 module from cell tips and cessation of polarized growth [5, 6]. We show that latrunculin A treatment also activates the Sty1 MAP kinase pathway and, strikingly, we find that loss of Sty1 MAP kinase signaling prevents latrunculin A-induced dispersal of the Cdc42 module, allowing polarized growth even in complete absence of the actin cytoskeleton. Regulation of the Cdc42 module by Sty1 is independent of Sty1’s role in stress-induced gene expression. We also describe a system for activation of Sty1 kinase “on demand” in the absence of any external stress, and use this to show that Sty1 activation alone is sufficient to disperse the Cdc42 module from cell tips in otherwise unperturbed cells. During nitrogen-starvation-induced quiescence, inhibition of Sty1 converts non-growing, depolarized cells into growing, polarized cells. Our results place MAP kinase Sty1 as an important physiological regulator of the Cdc42 polarity module.

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“…By contrast, fission yeast cells may align their spindle along the length of the cell primarily through the physical properties of microtubules. Despite early reports of a spindle orientation checkpoint (Gachet et al ., ; Oliferenko & Balasubramanian, ), more recent work found no evidence for such a checkpoint (Vogel et al ., ; Meadows & Millar, ). The spindles may be already prealigned at mitotic entry along the long cell axis through the action of interphase microtubules, which align along the long cell axis by sliding along the cell sides (Vogel et al ., ; Daga & Nurse, ).…”

Section: Generating Distinct Cells Shapesmentioning

confidence: 99%

Cell polarization in budding and fission yeasts

2014

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Polarization is a fundamental cellular property, which is essential for the function of numerous cell types. Over the past three to four decades, research using the best-established yeast systems in cell biological research, Saccharomyces cerevisiae (or budding yeast) and Schizosaccharomyces pombe (or fission yeast), has brought to light fundamental principles governing the establishment and maintenance of a polarized, asymmetric state. These two organisms, though both ascomycetes, are evolutionarily very distant and exhibit distinct shapes and modes of growth. In this review, we compare and contrast the two systems. We first highlight common cell polarization pathways, detailing the contribution of Rho GTPases, the cytoskeleton, membrane trafficking, lipids, and protein scaffolds. We then contrast the major differences between the two organisms, describing their distinct strategies in growth site selection and growth zone dimensions and compartmentalization, which may be the basis for their distinct shapes.

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Latrunculin A Delays Anaphase Onset in Fission Yeast by Disrupting an Ase1-independent Pathway Controlling Mitotic Spindle Stability

Cited by 21 publications

References 73 publications

Bub3p Facilitates Spindle Checkpoint Silencing in Fission Yeast

Bub3p Facilitates Spindle Checkpoint Silencing in Fission Yeast

Remodeling of the Fission Yeast Cdc42 Cell-Polarity Module via the Sty1 p38 Stress-Activated Protein Kinase Pathway

Cell polarization in budding and fission yeasts

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