Cell-cycle checkpoints that ensure coordination between nuclear and cytoplasmic events in Saccharomyces cerevisiae

2000 ◽  
Vol 10 (1) ◽  
pp. 47-53 ◽  
Author(s):  
Daniel J Lew
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Cell Cycle ◽  
Cell Cycle Checkpoints

scholarly journals Regulation of Mitotic Exit by Cell Cycle Checkpoints: Lessons From Saccharomyces cerevisiae

Genes ◽  
2020 ◽  
Vol 11 (2) ◽  
pp. 195 ◽  
Author(s):  
Laura Matellán ◽  
Fernando Monje-Casas
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Cell Cycle ◽  
Genome Stability ◽  
Molecular Mechanisms ◽  
Model Organism ◽  
Mitotic Exit ◽  
Cell Cycle Checkpoints ◽  
Dna Integrity ◽  
Intracellular Signals ◽  
Dividing Cells

In order to preserve genome integrity and their ploidy, cells must ensure that the duplicated genome has been faithfully replicated and evenly distributed before they complete their division by mitosis. To this end, cells have developed highly elaborated checkpoints that halt mitotic progression when problems in DNA integrity or chromosome segregation arise, providing them with time to fix these issues before advancing further into the cell cycle. Remarkably, exit from mitosis constitutes a key cell cycle transition that is targeted by the main mitotic checkpoints, despite these surveillance mechanisms being activated by specific intracellular signals and acting at different stages of cell division. Focusing primarily on research carried out using Saccharomyces cerevisiae as a model organism, the aim of this review is to provide a general overview of the molecular mechanisms by which the major cell cycle checkpoints control mitotic exit and to highlight the importance of the proper regulation of this process for the maintenance of genome stability during the distribution of the duplicated chromosomes between the dividing cells.

scholarly journals Reversibility of replicative senescence in Saccharomyces cerevisiae: Effect of homologous recombination and cell cycle checkpoints

DNA Repair ◽  
2012 ◽  
Vol 11 (1) ◽  
pp. 35-45 ◽  
Author(s):  
Sandra C. Becerra ◽  
Hiranthi T. Thambugala ◽  
Alison Russell Erickson ◽  
Christopher K. Lee ◽  
L. Kevin Lewis
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Cell Cycle ◽  
Homologous Recombination ◽  
Replicative Senescence ◽  
Cell Cycle Checkpoints

scholarly journals Microtubule Dynamics from Mating through the First Zygotic Division in the Budding Yeast Saccharomyces cerevisiae

1999 ◽  
Vol 144 (5) ◽  
pp. 977-987 ◽  
Author(s):  
Paul Maddox ◽  
E. Chin ◽  
A. Mallavarapu ◽  
E. Yeh ◽  
E.D. Salmon ◽  
...  
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Cell Cycle ◽  
Cell Fusion ◽  
Fluorescent Protein ◽  
Budding Yeast ◽  
Time Lapse ◽  
Spindle Pole ◽  
Microtubule Dynamics ◽  
Cell Cycle Checkpoints ◽  
Yeast Saccharomyces Cerevisiae

We have used time-lapse digital imaging microscopy to examine cytoplasmic astral microtubules (Mts) and spindle dynamics during the mating pathway in budding yeast Saccharomyces cerevisiae. Mating begins when two cells of opposite mating type come into proximity. The cells arrest in the G1 phase of the cell cycle and grow a projection towards one another forming a shmoo projection. Imaging of microtubule dynamics with green fluorescent protein (GFP) fusions to dynein or tubulin revealed that the nucleus and spindle pole body (SPB) became oriented and tethered to the shmoo tip by a Mt-dependent search and capture mechanism. Dynamically unstable astral Mts were captured at the shmoo tip forming a bundle of three or four astral Mts. This bundle changed length as the tethered nucleus and SPB oscillated toward and away from the shmoo tip at growth and shortening velocities typical of free plus end astral Mts (∼0.5 μm/min). Fluorescent fiduciary marks in Mt bundles showed that Mt growth and shortening occurred primarily at the shmoo tip, not the SPB. This indicates that Mt plus end assembly/disassembly was coupled to pushing and pulling of the nucleus. Upon cell fusion, a fluorescent bar of Mts was formed between the two shmoo tip bundles, which slowly shortened (0.23 ± 0.07 μm/min) as the two nuclei and their SPBs came together and fused (karyogamy). Bud emergence occurred adjacent to the fused SPB ∼30 min after SPB fusion. During the first mitosis, the SPBs separated as the spindle elongated at a constant velocity (0.75 μm/min) into the zygotic bud. There was no indication of a temporal delay at the 2-μm stage of spindle morphogenesis or a lag in Mt nucleation by replicated SPBs as occurs in vegetative mitosis implying a lack of normal checkpoints. Thus, the shmoo tip appears to be a new model system for studying Mt plus end dynamic attachments and much like higher eukaryotes, the first mitosis after haploid cell fusion in budding yeast may forgo cell cycle checkpoints present in vegetative mitosis.

Cancer Treatment with Liposomes Based Drugs and Genes Co-delivery Systems

2018 ◽  
Vol 25 (28) ◽  
pp. 3319-3332 ◽  
Author(s):  
Chuanmin Zhang ◽  
Shubiao Zhang ◽  
Defu Zhi ◽  
Jingnan Cui
Keyword(s):  
Cell Cycle ◽  
Cancer Cells ◽  
Synergistic Effects ◽  
Resistance Mechanisms ◽  
Delivery Systems ◽  
Cell Cycle Checkpoints ◽  
Drug Efflux ◽  
Cancer Resistance ◽  
Cancer Models ◽  
Anti Cancer

There are several mechanisms by which cancer cells develop resistance to treatments, including increasing anti-apoptosis, increasing drug efflux, inducing angiogenesis, enhancing DNA repair and altering cell cycle checkpoints. The drugs are hard to reach curative effects due to these resistance mechanisms. It has been suggested that liposomes based co-delivery systems, which can deliver drugs and genes to the same tumor cells and exhibit synergistic anti-cancer effects, could be used to overcome the resistance of cancer cells. As the co-delivery systems could simultaneously block two or more pathways, this might promote the death of cancer cells by sensitizing cells to death stimuli. This article provides a brief review on the liposomes based co-delivery systems to overcome cancer resistance by the synergistic effects of drugs and genes. Particularly, the synergistic effects of combinatorial anticancer drugs and genes in various cancer models employing multifunctional liposomes based co-delivery systems have been discussed. This review also gives new insights into the challenges of liposomes based co-delivery systems in the field of cancer therapy, by which we hope to provide some suggestions on the development of liposomes based co-delivery systems.

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