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.

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 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.

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 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.

Constitutive expression of the E2F1 transcription factor in fibroblasts alters G0 and S phase transit following serum stimulation

1996 ◽  
Vol 74 (1) ◽  
pp. 21-28 ◽  
Author(s):  
Thomas J. Logan ◽  
Kelly L. Jordan ◽  
David J. Hall
Keyword(s):  
Cell Cycle ◽  
Transcription Factor ◽  
Cell Lines ◽  
Constitutive Expression ◽  
S Phase ◽  
G1 Phase ◽  
Serum Starvation ◽  
Serum Stimulation ◽  
G0 Phase ◽  
E2f1 Transcription Factor

The E2F1 transcription factor was constitutively expressed in NIH3T3 fibroblasts to determine its effect on the cell cycle. These E2F1 cell lines were not tightly synchronized in G0 phase of the cell cycle following serum starvation, as are normal fibroblasts. Instead, the cells are spread throughout G0 and G1 phase with a portion of the population initiating DNA synthesis. Upon serum stimulation, the remaining cells in G0/G1 begin to enter S phase immediately but with a reduced rate. Constitutive expression of E2F1 appears to primarily affect the G0 phase, since transit of proliferating E2F1 cell lines through G1 phase is the same as control cells. Consistent with a shortened G0 phase, the E2F1 cell lines have a significantly reduced cellular volume. Additionally, the first S phase after serum stimulation, but not subsequent S phases, is nearly doubled in the E2F1 cell lines compared with control cells. Cell lines expressing a deletion mutant of E2F1 (termed E2F1d87), known to significantly affect cell shape, have cell cycle and volume characteristics similar to the E2F1 expressing cells. However, all S phase durations are considerably lengthened and the cells demonstrate delayed growth after plating.Key words: cell cycle, E2F1 transcription factor, G0/G1 phase.

scholarly journals Characterization of the Saccharomyces Golgi complex through the cell cycle by immunoelectron microscopy.

1992 ◽  
Vol 3 (7) ◽  
pp. 789-803 ◽  
Author(s):  
D Preuss ◽  
J Mulholland ◽  
A Franzusoff ◽  
N Segev ◽  
D Botstein
Keyword(s):  
Cell Cycle ◽  
Immunoelectron Microscopy ◽  
Early Stage ◽  
Secretory Vesicles ◽  
Wild Type ◽  
Daughter Cells ◽  
Bud Emergence ◽  
Membrane Compartments ◽  
Mother Cells

The membrane compartments responsible for Golgi functions in wild-type Saccharomyces cerevisiae were identified and characterized by immunoelectron microscopy. Using improved fixation methods, Golgi compartments were identified by labeling with antibodies specific for alpha 1-6 mannose linkages, the Sec7 protein, or the Ypt1 protein. The compartments labeled by each of these antibodies appear as disk-like structures that are apparently surrounded by small vesicles. Yeast Golgi typically are seen as single, isolated cisternae, generally not arranged into parallel stacks. The location of the Golgi structures was monitored by immunoelectron microscopy through the yeast cell cycle. Several Golgi compartments, apparently randomly distributed, were always observed in mother cells. During the initiation of new daughter cells, additional Golgi structures cluster just below the site of bud emergence. These Golgi enter daughter cells at an early stage, raising the possibility that much of the bud's growth might be due to secretory vesicles formed as well as consumed entirely within the daughter. During cytokinesis, the Golgi compartments are concentrated near the site of cell wall synthesis. Clustering of Golgi both at the site of bud formation and at the cell septum suggests that these organelles might be directed toward sites of rapid cell surface growth.

scholarly journals A preferred sequence for organelle inheritance during polarized cell growth

2021 ◽  
Author(s):  
Kathryn W. Li ◽  
Michelle S. Lu ◽  
Yuichiro Iwamoto ◽  
David G. Drubin ◽  
Ross T. A. Pedersen
Keyword(s):  
Cell Cycle ◽  
Cell Division ◽  
Cell Cycle Progression ◽  
Organelle Inheritance ◽  
Daughter Cells ◽  
Bud Emergence ◽  
Polarized Cell Growth ◽  
Bud Growth ◽  
Mother Cells ◽  
Cortical Endoplasmic Reticulum

Some organelles cannot be synthesized anew, so they are segregated into daughter cells during cell division. In Saccharomyces cerevisiae, daughter cells bud from mother cells and are populated by organelles inherited from the mothers. To determine whether this organelle inheritance occurs in a stereotyped manner, we tracked organelles using fluorescence microscopy. We describe a program for organelle inheritance in budding yeast. The cortical endoplasmic reticulum (ER) and peroxisomes are inherited concomitant with bud emergence. Next, vacuoles are inherited in small buds, followed closely by mitochondria. Finally, the nucleus and perinuclear ER are inherited when buds have nearly reached their maximal size. Because organelle inheritance timing correlates with bud morphology, which is coupled to the cell cycle, we tested whether disrupting the cell cycle alters organelle inheritance order. By arresting cell cycle progression but allowing continued bud growth, we determined that organelle inheritance still occurs when DNA replication is blocked, and that the general inheritance order is maintained. Thus, organelle inheritance follows a preferred order during polarized cell division and does not require completion of S-phase.

Cells and polyamines do it cyclically

2009 ◽  
Vol 46 ◽  
pp. 63-76 ◽  
Author(s):  
Kersti Alm ◽  
Stina Oredsson
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Progression ◽  
S Phase ◽  
Negative Regulator ◽  
Biosynthetic Activity ◽  
Polyamine Biosynthesis ◽  
Cycle Progression ◽  
Daughter Cells ◽  
G0 Phase ◽  
Proliferating Cell

Cell-cycle progression is a one-way journey where the cell grows in size to be able to divide into two equally sized daughter cells. The cell cycle is divided into distinct consecutive phases defined as G1 (first gap), S (synthesis), G2 (second gap) and M (mitosis). A non-proliferating cell, which has retained the ability to enter the cell cycle when it receives appropriate signals, is in G0 phase, and cycling cells that do not receive proper signals leave the cell cycle from G1 into G0. One of the major events of the cell cycle is the duplication of DNA during S-phase. A group of molecules that are important for proper cell-cycle progression is the polyamines. Polyamine biosynthesis occurs cyclically during the cell cycle with peaks in activity in conjunction with the G1/S transition and at the end of S-phase and during G2-phase. The negative regulator of polyamine biosynthesis, antizyme, shows an inverse activity compared with the polyamine biosynthetic activity. The levels of the polyamines, putrescine, spermidine and spermine, double during the cell cycle and show a certain degree of cyclic variation in accordance with the biosynthetic activity. When cells in G0/G1-phase are seeded in the presence of compounds that prevent the cell-cycle-related increases in the polyamine pools, the S-phase of the first cell cycle is prolonged, whereas the other phases are initially unaffected. The results point to an important role for polyamines with regard to the ability of the cell to attain optimal rates of DNA replication.

Cell Volume and the Control of the Chlamydomonas Cell Cycle

1982 ◽  
Vol 54 (1) ◽  
pp. 173-191 ◽  
Author(s):  
R. A. CRAIGIE ◽  
T. CAVALIER-SMITH
Keyword(s):  
Cell Cycle ◽  
Cell Wall ◽  
Cell Division ◽  
Simple Model ◽  
Cell Volume ◽  
Mother Cell ◽  
Dark Period ◽  
Size Fractions ◽  
Daughter Cells ◽  
Mother Cell Wall

Chlamydomonas reinhardii divides by multiple fission to produce 2n daughter cells per division burst, where n is an integer. By separating predivision cells from synchronous cultures into fractions of differing mean cell volumes, and electronically measuring the numbers and volume distributions of the daughter cells produced by the subsequent division burst, we have shown that n is determined by the volume of the parent cell. Control of n can occur simply, if after every cell division the daughter cells monitor their volume and divide again if, and only if, their volume is greater than a fixed minimum value. In cultures synchronized by 12-h light/12-h dark cycles, the larger parent cells divide earlier in the dark period than do smaller cells. This has been shown by two independent methods: (1) by separating cells into different size fractions by Percoll density-gradient centrifugation and using the light microscope to see when they divide; and (2) by studying changes in the cell volume distribution of unfractioned cultures. Since daughter cells remain within the mother-cell wall for some hours after cell division, and cell division causes an overall swelling of the mother-cell wall, the timing of division can be determined electronically by measuring this increase in cell volume that occurs in the dark period in the absence of growth; we find that cells at the large end of the size distribution range undergo this swelling first, and are then followed by successively smaller size fractions. A simple model embodying a sizer followed by a timer gives a good quantitative fit to these data for 12-h light/12-h dark cycles if cell division occurs 12-h after attaining a critical volume of approximately 140 μm3. However, this simple model is called into question by our finding that alterations in the length of the light period alter the rate of progress towards division even of cells that have attained their critical volume. We discuss the relative roles of light and cell volume in the control of division timing in the Chlamydomonas cell cycle.

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