Environmental control of cell size at division

Davie, Elizabeth A. Colby; Petersen, Janni

doi:10.1016/j.ceb.2012.08.003

Cited by 28 publications

(31 citation statements)

References 51 publications

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“…Fission yeast TOR kinases Tor1 and Tor2 are essential to coordinate cell growth and cell size within nutritional and environmental contexts (Davie and Petersen, 2012). Using a mutant expressing the thermosensitive allele of Tor2 (tor2-51), the core kinase of the TORC1 complex (Alvarez and Moreno, 2006), we found that Pmk1 activity was rather similar in cells incubated at permissive or restrictive temperatures under salt or cell wall stress (supplementary material Fig.…”

Section: Research Articlementioning

confidence: 93%

Multiple regulatory levels influence cell integrity control by PKC ortholog Pck2 in fission yeast

Madrid

Jiménez

Sánchez-Mir

et al. 2014

Journal of Cell Science

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The fission yeast protein kinase C (PKC) ortholog Pck2 controls cell wall synthesis and is a major upstream activator of the cell integrity pathway (CIP) and its core component, the MAP kinase Pmk1 (also known as Spm1), in response to environmental stimuli. We show that in vivo phosphorylation of Pck2 at the conserved T842 activation loop during growth and in response to different stresses is mediated by the phosphoinositide-dependent kinase (PDK) ortholog Ksg1 and an autophosphorylation mechanism. However, T842 phosphorylation is not essential for Pmk1 activation, and putative phosphorylation at T846 might play an additional role in Pck2 catalytic activation and downstream signaling. These events, together with turn motif autophosphorylation at T984 and binding to small GTPases Rho1 and/or Rho2, stabilize Pck2 and render it competent to exert its biological functions. Remarkably, the target of rapamycin complex 2 (TORC2) does not participate in the catalytic activation of Pck2, but instead contributes to de novo Pck2 synthesis, which is essential to activate the CIP in response to cell wall damage or glucose exhaustion. These results unveil a novel mechanism whereby TOR regulates PKC function at a translational level, and they add a new regulatory layer to MAPK signaling cascades.

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Section: Research Articlementioning

confidence: 93%

Multiple regulatory levels influence cell integrity control by PKC ortholog Pck2 in fission yeast

Madrid

Jiménez

Sánchez-Mir

et al. 2014

Journal of Cell Science

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“…There is abundant evidence for the coupling of proliferation and cell cycle progression to the nutrient environment and pH alteration [20], [41], [42]. We demonstrated that the exposure to the experimental group harvesting media (with relatively low nutrients or no pH buffer system) triggers p53-mediated cell cycle arrest and represses the expression of cyclin E1, eventually leading to the reduction of S-phase entry (Fig.…”

Section: Discussionmentioning

confidence: 80%

The Effects of Harvesting Media on Biological Characteristics and Repair Potential of Neural Stem Cells after Traumatic Brain Injury

Liu

et al. 2014

PLoS ONE

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Various solutions are utilized widely for the isolation, harvesting, sorting, testing and transplantation of neural stem cells (NSCs), whereas the effects of harvesting media on the biological characteristics and repair potential of NSCs remain unclear. To examine some of these effects, NSCs were isolated from cortex of E14.5 mice and exposed to the conventional harvesting media [0.9% saline (Saline), phosphate-buffered saline (PBS) or artificial cerebrospinal fluid (ACSF)] or the proliferation culture medium (PCM) for different durations at 4°C. Treated NSCs were grafted by in situ injection into the lesion sites of traumatic brain injury (TBI) mice. In vitro, harvesting media-exposed NSCs displayed time-dependent reduction of viability and proliferation. S phase entry decreased in harvesting media-exposed cells, which was associated with upregulation of p53 protein and downregulation of cyclin E1 protein. Moreover, harvesting media exposure induced the necrosis and apoptosis of NSCs. The levels of Fas-L, cleaved caspase 3 and 8 were increased, which suggests that the death receptor signaling pathway is involved in the apoptosis of NSCs. In addition, exposure to Saline did not facilitate the neuronal differentiation of NSCs, suggesting that Saline exposure may be disadvantageous for neurogenesis. In vivo, NSC-mediated functional recovery in harvesting media-exposed NSC groups was notably attenuated in comparison with the PCM-exposed NSC group. In conclusion, harvesting media exposure modulates the biological characteristics and repair potential of NSCs after TBI. Our results suggest that insight of the effects of harvesting media exposure on NSCs is critical for developing strategies to assure the successful long-term engraftment of NSCs.

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“…Conversely, limitations in nutritional environment restrain protein synthesis to conserve crucial metabolites and promote cell division to reduce size. Thus, cells constantly monitor nutrient availability and adjust cell growth and proliferation accordingly [1, 2]. The target of rapamycin (TOR) signalling pathway is integral to this coupling.…”

Section: Introductionmentioning

confidence: 99%

“…pombe , cell size control, after a shift from rich to poor nitrogen source (nitrogen stress), is dependent on TORC1 [1, 6–8]. The active TORC1 promotes cell growth to delay mitosis and cell division when good quality nutrients are present, whereas TORC1 activity decreases in response to a decline in nutrient quality and cells advance commitment to mitosis.…”

Section: Introductionmentioning

confidence: 99%

Ste12/Fab1 phosphatidylinositol-3-phosphate 5-kinase is required for nitrogen-regulated mitotic commitment and cell size control

et al. 2017

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Tight coupling of cell growth and cell cycle progression enable cells to adjust their rate of division, and therefore size, to the demands of proliferation in varying nutritional environments. Nutrient stress promotes inhibition of Target Of Rapamycin Complex 1 (TORC1) activity. In fission yeast, reduced TORC1 activity advances mitotic onset and switches growth to a sustained proliferation at reduced cell size. A screen for mutants, that failed to advance mitosis upon nitrogen stress, identified a mutant in the PIKFYVE 1-phosphatidylinositol-3-phosphate 5-kinase fission yeast homolog Ste12. Ste12PIKFYVE deficient mutants were unable to advance the cell cycle to reduce cell size after a nitrogen downshift to poor nitrogen (proline) growth conditions. While it is well established that PI(3,5)P2 signalling is required for autophagy and that Ste12PIKFYVE mutants have enlarged vacuoles (yeast lysosomes), neither a block to autophagy or mutants that independently have enlarged vacuoles had any impact upon nitrogen control of mitotic commitment. The addition of rapamycin to Ste12PIKFYVE deficient mutants reduced cell size at division to suggest that Ste12PIKFYVE possibly functions upstream of TORC1. ste12 mutants display increased Torin1 (TOR inhibitor) sensitivity. However, no major impact on TORC1 or TORC2 activity was observed in the ste12 deficient mutants. In summary, Ste12PIKFYVE is required for nitrogen-stress mediated advancement of mitosis to reduce cell size at division.

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Environmental control of cell size at division

Cited by 28 publications

References 51 publications

Multiple regulatory levels influence cell integrity control by PKC ortholog Pck2 in fission yeast

Multiple regulatory levels influence cell integrity control by PKC ortholog Pck2 in fission yeast

The Effects of Harvesting Media on Biological Characteristics and Repair Potential of Neural Stem Cells after Traumatic Brain Injury

Ste12/Fab1 phosphatidylinositol-3-phosphate 5-kinase is required for nitrogen-regulated mitotic commitment and cell size control

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