A nitrogen starvation-induced dormant G0 state in fission yeast: the establishment from uncommitted G1 state and its delay for return to proliferation

1996 ◽  
Vol 109 (6) ◽  
pp. 1347-1357 ◽  
Author(s):  
S.S. Su ◽  
Y. Tanaka ◽  
I. Samejima ◽  
K. Tanaka ◽  
M. Yanagida
Keyword(s):  
Cell Division ◽  
Fission Yeast ◽  
Cell Shape ◽  
Nitrogen Starvation ◽  
Stable State ◽  
Mitotic Cell ◽  
Yeast Cells ◽  
Dormant Cells ◽  
State Dependent ◽  
G1 Cells

Fission yeast cells either remain in the mitotic cell cycle or exit to meiotic sporulation from an uncommitted G1 state dependent on the presence or absence of nitrogen source in the medium (Nurse and Bissett, 1981). We examined how heterothallic haploid cells, which cannot sporulate, behave under nitrogen-starvation for longer than 25 days at 26 degrees C. These cells were shown to enter a stable state (designated the dormant G0) with nearly full viability. Maintaining the dormant cells required glucose, suggesting that the cells remained metabolically active although cell division had ceased. They differed dramatically from mitotic and uncommitted G1 cells in heat resistance, and also in cytoplasmic and nuclear morphologies. After nitrogen replenishment, the initial responses of dormant G0 cells were investigated. The kinetics for reentry into the proliferative state were delayed considerably, and the changes in cell shape were enhanced particularly for those recovering from extended nitrogen starvation. A part of the delay could be accounted for by the duration of nuclear decondensation and cell elongation for the first cell division.

scholarly journals Apical Constriction Reversal upon Mitotic Entry Underlies Different Morphogenetic Outcomes of Cell Division

2019 ◽  
Author(s):  
Clint S. Ko ◽  
Prateek Kalakuntla ◽  
Adam C. Martin
Keyword(s):  
Cell Division ◽  
Cell Shape ◽  
Mitotic Cell ◽  
Signal Interference ◽  
Apical Constriction ◽  
Mitotic Entry ◽  
Cell Divisions ◽  
Cell Shape Changes ◽  
Shape Changes ◽  
Mitotic Cells

AbstractDuring development, coordinated cell shape changes and cell divisions sculpt tissues. While these individual cell behaviors have been extensively studied, how cell shape changes and cell divisions that occur concurrently in epithelia influence tissue shape is less understood. We addressed this question in two contexts of the early Drosophila embryo: premature cell division during mesoderm invagination, and native ectodermal cell divisions with ectopic activation of apical contractility. Using quantitative live-cell imaging, we demonstrated that mitotic entry reverses apical contractility by interfering with medioapical RhoA signaling. While premature mitotic entry inhibits mesoderm invagination, which relies on apical constriction, mitotic entry in an artificially contractile ectoderm induced ectopic tissue invaginations. Ectopic invaginations resulted from medioapical myosin loss in neighboring mitotic cells. This myosin loss enabled non-mitotic cells to apically constrict through mitotic cell stretching. Thus, the spatial pattern of mitotic entry can differentially regulate tissue shape through signal interference between apical contractility and mitosis.

scholarly journals Cell Shape and Cell Division in Fission Yeast

2009 ◽  
Vol 19 (17) ◽  
pp. R823-R827 ◽  
Author(s):  
Matthieu Piel ◽  
Phong T. Tran
Keyword(s):  
Cell Division ◽  
Fission Yeast ◽  
Cell Shape

Microtubule Architectural Dynamics Determine Cell Shape and Cell Division Site in Fission Yeast

2004 ◽  
Vol 10 (S02) ◽  
pp. 162-163
Author(s):  
Isabelle Loiodice ◽  
Marcel E. Janson ◽  
Jamye Staub ◽  
Thanuja Gangi-Setty ◽  
Nam P. Nguyen ◽  
...  
Keyword(s):  
Cell Division ◽  
Fission Yeast ◽  
Cell Shape ◽  
Division Site

Extended abstract of a paper presented at Microscopy and Microanalysis 2004 in Savannah, Georgia, USA, August 1–5, 2004.

Genes for a Nuclease and a Protease Are Involved in the Drastic Decrease in Cellular RNA Amount in Fission Yeast Cells during Nitrogen Starvation

2002 ◽  
Vol 131 (3) ◽  
pp. 391-398 ◽  
Author(s):  
A. Nakashima ◽  
M. Yoshida ◽  
K. Nakayama ◽  
A. Kato-Furuno ◽  
M. Ueno ◽  
...  
Keyword(s):  
Fission Yeast ◽  
Nitrogen Starvation ◽  
Yeast Cells ◽  
Drastic Decrease

scholarly journals Combined effect of cell geometry and polarity domains determines the orientation of unequal division

eLife ◽  
2021 ◽  
Vol 10 ◽  
Author(s):  
Benoit G Godard ◽  
Remi Dumollard ◽  
Carl-Philipp Heisenberg ◽  
Alex McDougall
Keyword(s):  
Cell Division ◽  
Mitotic Spindle ◽  
Cell Shape ◽  
Daughter Cell ◽  
Cleavage Plane ◽  
Mitotic Cell ◽  
Cell Geometry ◽  
Daughter Cells ◽  
Ascidian Embryos ◽  
Spindle Position

Cell division orientation is thought to result from a competition between cell geometry and polarity domains controlling the position of the mitotic spindle during mitosis. Depending on the level of cell shape anisotropy or the strength of the polarity domain, one dominates the other and determines the orientation of the spindle. Whether and how such competition is also at work to determine unequal cell division (UCD), producing daughter cells of different size, remains unclear. Here, we show that cell geometry and polarity domains cooperate, rather than compete, in positioning the cleavage plane during UCDs in early ascidian embryos. We found that the UCDs and their orientation at the ascidian third cleavage rely on the spindle tilting in an anisotropic cell shape, and cortical polarity domains exerting different effects on spindle astral microtubules. By systematically varying mitotic cell shape, we could modulate the effect of attractive and repulsive polarity domains and consequently generate predicted daughter cell size asymmetries and position. We therefore propose that the spindle position during UCD is set by the combined activities of cell geometry and polarity domains, where cell geometry modulates the effect of cortical polarity domain(s).

scholarly journals Schizosaccharomyces pombe Noc3 Is Essential for Ribosome Biogenesis and Cell Division but Not DNA Replication

2008 ◽  
Vol 7 (9) ◽  
pp. 1433-1440 ◽  
Author(s):  
Christopher R. Houchens ◽  
Audrey Perreault ◽  
François Bachand ◽  
Thomas J. Kelly
Keyword(s):  
Cell Division ◽  
Dna Replication ◽  
Schizosaccharomyces Pombe ◽  
Fission Yeast ◽  
Ribosome Biogenesis ◽  
Budding Yeast ◽  
Ribosomal Subunit ◽  
Dna Helicase ◽  
Yeast Cells ◽  
Direct Role

ABSTRACT The initiation of eukaryotic DNA replication is preceded by the assembly of prereplication complexes (pre-RCs) at chromosomal origins of DNA replication. Pre-RC assembly requires the essential DNA replication proteins ORC, Cdc6, and Cdt1 to load the MCM DNA helicase onto chromatin. Saccharomyces cerevisiae Noc3 (ScNoc3), an evolutionarily conserved protein originally implicated in 60S ribosomal subunit trafficking, has been proposed to be an essential regulator of DNA replication that plays a direct role during pre-RC formation in budding yeast. We have cloned Schizosaccharomyces pombe noc3 + (Spnoc3 +), the S. pombe homolog of the budding yeast ScNOC3 gene, and functionally characterized the requirement for the SpNoc3 protein during ribosome biogenesis, cell cycle progression, and DNA replication in fission yeast. We showed that fission yeast SpNoc3 is a functional homolog of budding yeast ScNoc3 that is essential for cell viability and ribosome biogenesis. We also showed that SpNoc3 is required for the normal completion of cell division in fission yeast. However, in contrast to the proposal that ScNoc3 plays an essential role during DNA replication in budding yeast, we demonstrated that fission yeast cells do enter and complete S phase in the absence of SpNoc3, suggesting that SpNoc3 is not essential for DNA replication in fission yeast.

scholarly journals Molecular networks linked by Moesin drive remodeling of the cell cortex during mitosis

2011 ◽  
Vol 195 (1) ◽  
pp. 99-112 ◽  
Author(s):  
Chantal Roubinet ◽  
Barbara Decelle ◽  
Gaëtan Chicanne ◽  
Jonas F. Dorn ◽  
Bernard Payrastre ◽  
...  
Keyword(s):  
Cell Division ◽  
Cell Elongation ◽  
Cell Shape ◽  
Mitotic Cell ◽  
Molecular Networks ◽  
Cell Cortex ◽  
Anaphase Onset ◽  
Shape Transformations ◽  
Intracellular Pressure ◽  
Early Mitosis

The cortical mechanisms that drive the series of mitotic cell shape transformations remain elusive. In this paper, we identify two novel networks that collectively control the dynamic reorganization of the mitotic cortex. We demonstrate that Moesin, an actin/membrane linker, integrates these two networks to synergize the cortical forces that drive mitotic cell shape transformations. We find that the Pp1-87B phosphatase restricts high Moesin activity to early mitosis and down-regulates Moesin at the polar cortex, after anaphase onset. Overactivation of Moesin at the polar cortex impairs cell elongation and thus cytokinesis, whereas a transient recruitment of Moesin is required to retract polar blebs that allow cortical relaxation and dissipation of intracellular pressure. This fine balance of Moesin activity is further adjusted by Skittles and Pten, two enzymes that locally produce phosphoinositol 4,5-bisphosphate and thereby, regulate Moesin cortical association. These complementary pathways provide a spatiotemporal framework to explain how the cell cortex is remodeled throughout cell division.

scholarly journals The phosphatase inhibitor Sds23 regulates cell division symmetry in fission yeast

2019 ◽  
Author(s):  
Katherine L. Schutt ◽  
James B. Moseley
Keyword(s):  
Cell Division ◽  
Fission Yeast ◽  
Cell Polarity ◽  
Protein Phosphatase ◽  
Yeast Cells ◽  
Spatial Control ◽  
Anchoring Proteins ◽  
Family Protein ◽  
Mutant Cells ◽  
Assembly Site

AbstractAnimal and fungal cells divide through the assembly, anchoring, and constriction of a contractile actomyosin ring (CAR) during cytokinesis. The timing and position of the CAR must be tightly controlled to prevent defects in cell division, but many of the underlying signaling events remain unknown. The conserved heterotrimeric protein phosphatase PP2A controls the timing of events in mitosis, and upstream pathways including Greatwall-Ensa regulate PP2A activity. A role for PP2A in CAR regulation has been less clear, although loss of PP2A in yeast causes defects in cytokinesis. Here, we report that Sds23, an inhibitor of PP2A family protein phosphatases, promotes the symmetric division of fission yeast cells through spatial control of cytokinesis. We found that sds23Δ cells divide asymmetrically due to misplaced CAR assembly, followed by sliding of the CAR away from its assembly site. These mutant cells exhibit delayed recruitment of putative CAR anchoring proteins including the glucan synthase Bgs1. Our observations likely reflect a broader role for regulation of PP2A in cell polarity and cytokinesis because sds23Δ phenotypes were exacerbated when combined with mutations in the fission yeast Ensa homolog, Igo1. These results identify the PP2A regulatory network as a critical component in the signaling pathways coordinating cytokinesis.

scholarly journals The phosphatase inhibitor Sds23 regulates cell division symmetry in fission yeast

2019 ◽  
Vol 30 (23) ◽  
pp. 2880-2889 ◽  
Author(s):  
Katherine L. Schutt ◽  
James B. Moseley
Keyword(s):  
Cell Division ◽  
Fission Yeast ◽  
Cell Polarity ◽  
Protein Phosphatase ◽  
Yeast Cells ◽  
Spatial Control ◽  
Anchoring Proteins ◽  
Family Protein ◽  
Mutant Cells ◽  
Assembly Site

Animal and fungal cells divide through the assembly, anchoring, and constriction of a contractile actomyosin ring (CAR) during cytokinesis. The timing and position of the CAR must be tightly controlled to prevent defects in cell division, but many of the underlying signaling events remain unknown. The conserved heterotrimeric protein phosphatase PP2A controls the timing of events in mitosis, and upstream pathways including Greatwall–Ensa regulate PP2A activity. A role for PP2A in CAR regulation has been less clear, although loss of PP2A in yeast causes defects in cytokinesis. Here, we report that Sds23, an inhibitor of PP2A family protein phosphatases, promotes the symmetric division of fission yeast cells through spatial control of cytokinesis. We found that sds23∆ cells divide asymmetrically due to misplaced CAR assembly, followed by sliding of the CAR away from its assembly site. These mutant cells exhibit delayed recruitment of putative CAR anchoring proteins including the glucan synthase Bgs1. Our observations likely reflect a broader role for regulation of PP2A in cell polarity and cytokinesis because sds23∆ phenotypes were exacerbated when combined with mutations in the fission yeast Ensa homologue, Igo1. These results identify the PP2A regulatory network as a critical component in the signaling pathways coordinating cytokinesis.

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