scholarly journals Temporal integration of mitogen history in mother cells controls proliferation of daughter cells

Science ◽  
2020 ◽  
Vol 368 (6496) ◽  
pp. 1261-1265 ◽  
Author(s):  
Mingwei Min ◽  
Yao Rong ◽  
Chengzhe Tian ◽  
Sabrina L. Spencer
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Mother Cell ◽  
Protein Production ◽  
Temporal Integration ◽  
Protein Translation ◽  
Cycle Phase ◽  
Daughter Cells ◽  
Mother Cells ◽  
Multicellular Organisms

Multicellular organisms use mitogens to regulate cell proliferation, but how fluctuating mitogenic signals are converted into proliferation-quiescence decisions is poorly understood. In this work, we combined live-cell imaging with temporally controlled perturbations to determine the time scale and mechanisms underlying this system in human cells. Contrary to the textbook model that cells sense mitogen availability only in the G1 cell cycle phase, we find that mitogenic signaling is temporally integrated throughout the entire mother cell cycle and that even a 1-hour lapse in mitogen signaling can influence cell proliferation more than 12 hours later. Protein translation rates serve as the integrator that proportionally converts mitogen history into corresponding levels of cyclin D in the G2 phase of the mother cell, which controls the proliferation-quiescence decision in daughter cells and thereby couples protein production with cell proliferation.

scholarly journals Cell cycle phases in the unequal mother/daughter cell cycles of Saccharomyces cerevisiae.

1984 ◽  
Vol 4 (11) ◽  
pp. 2529-2531 ◽  
Author(s):  
B J Brewer ◽  
E Chlebowicz-Sledziewska ◽  
W L Fangman
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Cell Cycle ◽  
Cycle Phase ◽  
Cell Cycle Time ◽  
Yeast Saccharomyces Cerevisiae ◽  
Cell Cycles ◽  
Daughter Cells ◽  
Mother And Daughter ◽  
Cell Cycle Phases ◽  
Mother Cells

During cell division in the yeast Saccharomyces cerevisiae mother cells produce buds (daughter cells) which are smaller and have longer cell cycles. We performed experiments to compare the lengths of cell cycle phases in mothers and daughters. As anticipated from earlier indirect observations, the longer cell cycle time of daughter cells is accounted for by a longer G1 interval. The S-phase and the G2-phase are of the same duration in mother and daughter cells. An analysis of five isogenic strains shows that cell cycle phase lengths are independent of cell ploidy and mating type.

scholarly journals The fate of notch-1 transcript is linked to cell cycle dynamics by activity of a natural antisense transcript

2021 ◽  
Vol 49 (18) ◽  
pp. 10419-10430
Author(s):  
Filip Vujovic ◽  
Saba Rezaei-Lotfi ◽  
Neil Hunter ◽  
Ramin M Farahani
Keyword(s):  
Cell Cycle ◽  
Mother Cell ◽  
Antisense Transcript ◽  
Cell Lineage ◽  
G1 Phase ◽  
Natural Antisense Transcript ◽  
Notch 1 ◽  
Daughter Cells ◽  
G0 Phase ◽  
Mother Cells

Abstract A core imprint of metazoan life is that perturbations of cell cycle are offset by compensatory changes in successive cellular generations. This trait enhances robustness of multicellular growth and requires transmission of signaling cues within a cell lineage. Notably, the identity and mode of activity of transgenerational signals remain largely unknown. Here we report the discovery of a natural antisense transcript encoded in exon 25 of notch-1 locus (nAS25) by which mother cells control the fate of notch-1 transcript in daughter cells to buffer against perturbations of cell cycle. The antisense transcript is transcribed at G1 phase of cell cycle from a bi-directional E2F1-dependent promoter in the mother cell where the titer of nAS25 is calibrated to the length of G1. Transmission of the antisense transcript from mother to daughter cells stabilizes notch-1 sense transcript in G0 phase of daughter cells by masking it from RNA editing and resultant nonsense-mediated degradation. In consequence, nAS25-mediated amplification of notch-1 signaling reprograms G1 phase in daughter cells to compensate for the altered dynamics of the mother cell. The function of nAS25/notch-1 in integrating G1 phase history of the mother cell into that of daughter cells is compatible with the predicted activity of a molecular oscillator, slower than cyclins, that coordinates cell cycle within cell lineage.

Cell cycle phases in the unequal mother/daughter cell cycles of Saccharomyces cerevisiae

1984 ◽  
Vol 4 (11) ◽  
pp. 2529-2531
Author(s):  
B J Brewer ◽  
E Chlebowicz-Sledziewska ◽  
W L Fangman
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Cell Cycle ◽  
Cycle Phase ◽  
Cell Cycle Time ◽  
Yeast Saccharomyces Cerevisiae ◽  
Cell Cycles ◽  
Daughter Cells ◽  
Mother And Daughter ◽  
Cell Cycle Phases ◽  
Mother Cells

During cell division in the yeast Saccharomyces cerevisiae mother cells produce buds (daughter cells) which are smaller and have longer cell cycles. We performed experiments to compare the lengths of cell cycle phases in mothers and daughters. As anticipated from earlier indirect observations, the longer cell cycle time of daughter cells is accounted for by a longer G1 interval. The S-phase and the G2-phase are of the same duration in mother and daughter cells. An analysis of five isogenic strains shows that cell cycle phase lengths are independent of cell ploidy and mating type.

scholarly journals Loss of MCU prevents mitochondrial fusion in G1-S phase and blocks cell cycle progression and proliferation

2019 ◽  
Vol 12 (579) ◽  
pp. eaav1439 ◽  
Author(s):  
Olha M. Koval ◽  
Emily K. Nguyen ◽  
Velarchana Santhana ◽  
Trevor P. Fidler ◽  
Sara C. Sebag ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Cell Cycle Progression ◽  
Mitochondrial Fission ◽  
Mitochondrial Fusion ◽  
Cycle Phase ◽  
Wild Type ◽  
Mitochondrial Fragmentation ◽  
Cycle Progression ◽  
Regulatory Circuit

The role of the mitochondrial Ca2+uniporter (MCU) in physiologic cell proliferation remains to be defined. Here, we demonstrated that the MCU was required to match mitochondrial function to metabolic demands during the cell cycle. During the G1-S transition (the cycle phase with the highest mitochondrial ATP output), mitochondrial fusion, oxygen consumption, and Ca2+uptake increased in wild-type cells but not in cells lacking MCU. In proliferating wild-type control cells, the addition of the growth factors promoted the activation of the Ca2+/calmodulin-dependent kinase II (CaMKII) and the phosphorylation of the mitochondrial fission factor Drp1 at Ser616. The lack of the MCU was associated with baseline activation of CaMKII, mitochondrial fragmentation due to increased Drp1 phosphorylation, and impaired mitochondrial respiration and glycolysis. The mitochondrial fission/fusion ratio and proliferation in MCU-deficient cells recovered after MCU restoration or inhibition of mitochondrial fragmentation or of CaMKII in the cytosol. Our data highlight a key function for the MCU in mitochondrial adaptation to the metabolic demands during cell cycle progression. Cytosolic CaMKII and the MCU participate in a regulatory circuit, whereby mitochondrial Ca2+uptake affects cell proliferation through Drp1.

scholarly journals The ER Stress Surveillance (ERSU) pathway regulates daughter cell ER protein aggregate inheritance

eLife ◽  
2015 ◽  
Vol 4 ◽  
Author(s):  
Francisco J Piña ◽  
Maho Niwa
Keyword(s):  
Cell Cycle ◽  
Endoplasmic Reticulum ◽  
Er Stress ◽  
Mother Cell ◽  
Daughter Cell ◽  
Protein Aggregates ◽  
Cytoplasmic Protein ◽  
Protein Aggregate ◽  
Daughter Cells ◽  
Simultaneous Visualization

Stress induced by cytoplasmic protein aggregates can have deleterious consequences for the cell, contributing to neurodegeneration and other diseases. Protein aggregates are also formed within the endoplasmic reticulum (ER), although the fate of ER protein aggregates, specifically during cell division, is not well understood. By simultaneous visualization of both the ER itself and ER protein aggregates, we found that ER protein aggregates that induce ER stress are retained in the mother cell by activation of the ER Stress Surveillance (ERSU) pathway, which prevents inheritance of stressed ER. In contrast, under conditions of normal ER inheritance, ER protein aggregates can enter the daughter cell. Thus, whereas cytoplasmic protein aggregates are retained in the mother cell to protect the functional capacity of daughter cells, the fate of ER protein aggregates is determined by whether or not they activate the ERSU pathway to impede transmission of the cortical ER during the cell cycle.

Silencing of miR-1246 Induces Cell Cycle Arrest and Apoptosis in Cisplatin-Resistant Ovarian Cancer Cells by Promoting ZNF23 Transcription

2021 ◽  
pp. 1-13
Author(s):  
Lu Cai ◽  
Qian Zhang ◽  
Lili Du ◽  
Feiyun Zheng
Keyword(s):  
Cell Cycle ◽  
Ovarian Cancer ◽  
Cell Proliferation ◽  
Cell Cycle Arrest ◽  
Cell Cycle Progression ◽  
Luciferase Reporter ◽  
Cycle Phase ◽  
Ovarian Cancer Cells ◽  
Tunel Staining ◽  
Cycle Arrest

Ovarian cancer (OC) is the most frequent cause of death among patients with gynecologic malignancies. In recent years, the development of cisplatin (DDP) resistance has become an important reason for the poor prognosis of OC patients. Therefore, it is vital to explore the mechanism of DDP resistance in OC. In this study, microRNA-1246 (miR-1246) expression in OC and DDP-resistant OC cells was determined by RT-qPCR, and chemosensitivity to DDP was assessed by the CCK-8 assay. A dual-luciferase reporter assay was performed to confirm the interaction between miR-1246 and zinc finger 23 (<i>ZNF23</i>), while changes in <i>ZNF23</i> expression were monitored by RT-qPCR, immunofluorescence, and western blot assays. Moreover, cell proliferation, cycle phase, and apoptosis were determined by EdU staining, flow cytometry, TUNEL staining, and Hoechst staining. Our data showed that miR-1246 was highly expressed in DDP-resistant OVCAR-3 and TOV-112D cells. Functionally, overexpression of miR-1246 markedly enhanced DDP resistance and cell proliferation, and suppressed cell cycle arrest and apoptosis of OC cells. Inhibition of miR-1246 expression significantly attenuated DDP resistance and cell proliferation, and increased cell cycle arrest and apoptosis in DDP-resistant OC cells. Furthermore, <i>ZNF23</i> was identified as a target gene of miR-1246, and ZNF23 protein expression was notably downregulated in DDP-resistant OC cells. Moreover, overexpression of miR-1246 significantly downregulated the <i>ZNF23</i> levels in OVCAR-3 and TOV-112D cells, and inhibition of miR-1246 upregulated the <i>ZNF23</i> levels in the DDP-resistant OVCAR-3 and TOV-112D cells. In conclusion, miR-1246 might be a novel regulator of DDP-resistant OC that functions by regulating <i>ZNF23</i> expression in DDP-resistant cells, as well as cell proliferation, cell cycle progression, and apoptosis.

PCNA and total nuclear protein content as markers of cell proliferation in pea tissue

1992 ◽  
Vol 102 (1) ◽  
pp. 71-78 ◽  
Author(s):  
SANDRA CITTERIO ◽  
SERGIO SGORBATI ◽  
MARISA LEVI ◽  
BRUNO MARIA COLOMBO ◽  
ELIO SPARVOLI
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Protein Content ◽  
Time Course ◽  
Nuclear Protein ◽  
Flow Cytometric Analysis ◽  
Nuclear Antigen ◽  
Cycle Phase ◽  
Proliferating Cells ◽  
Embryo Cells

The identification of cell proliferation markers has been shown to be a useful tool with which to study basic mechanisms of cell cycle progression. The use of immunofluorescence techniques revealed the presence of the proliferating cell nuclear antigen (PCNA) in pea tissue, where we observed a high PCNA expression in proliferating cells of the root meristem compared to noncycling cells of the differentiated leaf. The presence of PCNA was monitored also during the time-course of seed germination, before, during and after the cell cycle resumption of the embryo cells. PCNA is present in embryo cells not only during and after resumption of the cell cycle but also before, when cells have not yet begun replicating their genome. A bivariate flow cytometric analysis of DNA and nuclear protein content was used to localize precisely the cells of the examined pea tissues in different cell cycle phase subcompartments. A high correlation was found between the degree of cell proliferation and the protein content of G1 nuclei, on the one hand, and the percentage of PCNA positive cells on the other.

scholarly journals The effects of 5α-dihydrotestosterone on the kinetics of cell proliferation in rat prostate

1974 ◽  
Vol 142 (3) ◽  
pp. 483-489 ◽  
Author(s):  
Barry Lesser ◽  
Nicholas Bruchovsky
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Cellular Growth ◽  
Velocity Sedimentation ◽  
Growth Fraction ◽  
Subcutaneous Injections ◽  
Daughter Cells ◽  
A Cell ◽  
Rat Prostate ◽  
Kinetics Of

The regenerating rat prostate was used as an experimental model to determine the effects of 5α-dihydrotestosterone on certain parameters of cell proliferation, including the duration of the phases of the cell cycle and the size of the cellular growth fraction. Rats castrated 7 days previously were treated with daily subcutaneous injections of 5α-dihydrotestosterone for 14 days; 48h after the beginning of therapy, cells in the process of DNA synthesis were labelled with a single injection of radioactive thymidine and the progress of these cells through the division cycle was observed. Cell-cycle analysis was performed by fractionating prostatic nuclei according to their position in the cell cycle by using the technique of velocity sedimentation under unit gravity. The results indicate that during regeneration the cell population undergoes 1.8 doublings with a doubling time of 40h, and that the process involves almost four rounds of cell division with a cell-generation time of 20h. The growth fraction at any time is about 0.5, and about half the daughter cells produced do not re-enter the proliferative cycle. All cells present at the start of regeneration eventually undergo at least one division during the course of regeneration, although any given cell can divide from one to four times.

scholarly journals Epigenetic Regulation of Plant Gametophyte Development

2019 ◽  
Vol 20 (12) ◽  
pp. 3051 ◽  
Author(s):  
Vasily V. Ashapkin ◽  
Lyudmila I. Kutueva ◽  
Nadezhda I. Aleksandrushkina ◽  
Boris F. Vanyushin
Keyword(s):  
Mother Cell ◽  
Female Gametophyte ◽  
Male Gametophyte ◽  
Endosperm Development ◽  
Epigenetic Changes ◽  
Gametophyte Development ◽  
Daughter Cells ◽  
Second Stage ◽  
Somatic Tissues ◽  
Mother Cells

Unlike in animals, the reproductive lineage cells in plants differentiate from within somatic tissues late in development to produce a specific haploid generation of the life cycle—male and female gametophytes. In flowering plants, the male gametophyte develops within the anthers and the female gametophyte—within the ovule. Both gametophytes consist of only a few cells. There are two major stages of gametophyte development—meiotic and post-meiotic. In the first stage, sporocyte mother cells differentiate within the anther (pollen mother cell) and the ovule (megaspore mother cell). These sporocyte mother cells undergo two meiotic divisions to produce four haploid daughter cells—male spores (microspores) and female spores (megaspores). In the second stage, the haploid spore cells undergo few asymmetric haploid mitotic divisions to produce the 3-cell male or 7-cell female gametophyte. Both stages of gametophyte development involve extensive epigenetic reprogramming, including siRNA dependent changes in DNA methylation and chromatin restructuring. This intricate mosaic of epigenetic changes determines, to a great extent, embryo and endosperm development in the future sporophyte generation.

scholarly journals Myosin-driven peroxisome partitioning in S. cerevisiae

2009 ◽  
Vol 186 (4) ◽  
pp. 541-554 ◽  
Author(s):  
Andrei Fagarasanu ◽  
Fred D. Mast ◽  
Barbara Knoblach ◽  
Yui Jin ◽  
Matthew J. Brunner ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Molecular Motors ◽  
Cell Cycle Progression ◽  
Cycle Progression ◽  
Class V ◽  
Daughter Cells ◽  
Mother And Daughter ◽  
Specific Receptors ◽  
Cycle Dependent ◽  
Mother Cells

In Saccharomyces cerevisiae, the class V myosin motor Myo2p propels the movement of most organelles. We recently identified Inp2p as the peroxisome-specific receptor for Myo2p. In this study, we delineate the region of Myo2p devoted to binding peroxisomes. Using mutants of Myo2p specifically impaired in peroxisome binding, we dissect cell cycle–dependent and peroxisome partitioning–dependent mechanisms of Inp2p regulation. We find that although total Inp2p levels oscillate with the cell cycle, Inp2p levels on individual peroxisomes are controlled by peroxisome inheritance, as Inp2p aberrantly accumulates and decorates all peroxisomes in mother cells when peroxisome partitioning is abolished. We also find that Inp2p is a phosphoprotein whose level of phosphorylation is coupled to the cell cycle irrespective of peroxisome positioning in the cell. Our findings demonstrate that both organelle positioning and cell cycle progression control the levels of organelle-specific receptors for molecular motors to ultimately achieve an equidistribution of compartments between mother and daughter cells.

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