scholarly journals Mitotic Cyclins Regulate Telomeric Recombination in Telomerase-Deficient Yeast Cells

2003 ◽  
Vol 23 (24) ◽  
pp. 9162-9177 ◽  
Author(s):  
Nathalie Grandin ◽  
Michel Charbonneau
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Genetic Interaction ◽  
Mitotic Cell ◽  
Nuclease Activity ◽  
Yeast Cells ◽  
Growth Defect ◽  
Mitotic Cell Cycle ◽  
Functional Interaction ◽  
Synthetic Growth

ABSTRACT Telomerase-deficient mutants of Saccharomyces cerevisiae can survive death by senescence by using one of two homologous recombination pathways. The Rad51 pathway amplifies the subtelomeric Y′ sequences, while the Rad50 pathway amplifies the telomeric TG1-3 repeats. Here we show that telomerase-negative cells require Clb2 (the major B-type cyclin in this organism), in association with Cdc28 (Cdk1), to generate postsenescence survivors at a normal rate. The Rad50 pathway was more sensitive to the absence of Clb2 than the Rad51 pathway. We also report that telomerase RAD50 RAD51 triple mutants still generated postsenescence survivors. This novel Rad50- and Rad51-independent pathway of telomeric recombination also appeared to be controlled by Clb2. In telomerase-positive cells, a synthetic growth defect between mutations in CLB2 and RAD50 or in its partners in the conserved MRX complex, MRE11 and XRS2, was observed. This genetic interaction was independent of Mre11 nuclease activity but was dependent on a DNA repair function. The present data reveal an unexpected role of Cdc28/Clb2 in telomeric recombination during telomerase-independent maintenance of telomeres. They also uncover a functional interaction between Cdc28/Clb2 and MRX during the control of the mitotic cell cycle.

The Saccharomyces cerevisiae DNA repair gene RAD2 is regulated in meiosis but not during the mitotic cell cycle

1990 ◽  
Vol 10 (6) ◽  
pp. 3256-3257
Author(s):  
K Madura ◽  
S Prakash
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Cell Cycle ◽  
Dna Damage ◽  
Mitotic Cell ◽  
Mitotic Cell Cycle ◽  
Repair Gene ◽  
Mrna Accumulation ◽  
Transcript Levels ◽  
Dna Repair Gene

The expression of the RAD2 gene of Saccharomyces cerevisiae is elevated upon DNA damage. Here, we show that RAD2 transcript levels also rise approximately eightfold during meiosis but remain constant during the mitotic cell cycle. The period of maximal RAD2 mRNA accumulation during meiosis is consistent with a possible role of RAD2 in a late stage of recombination, in mismatch repair of heteroduplexes, or both.

scholarly journals The Saccharomyces cerevisiae DNA repair gene RAD2 is regulated in meiosis but not during the mitotic cell cycle.

1990 ◽  
Vol 10 (6) ◽  
pp. 3256-3257 ◽  
Author(s):  
K Madura ◽  
S Prakash
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Cell Cycle ◽  
Dna Damage ◽  
Mitotic Cell ◽  
Mitotic Cell Cycle ◽  
Repair Gene ◽  
Mrna Accumulation ◽  
Transcript Levels ◽  
Dna Repair Gene

The expression of the RAD2 gene of Saccharomyces cerevisiae is elevated upon DNA damage. Here, we show that RAD2 transcript levels also rise approximately eightfold during meiosis but remain constant during the mitotic cell cycle. The period of maximal RAD2 mRNA accumulation during meiosis is consistent with a possible role of RAD2 in a late stage of recombination, in mismatch repair of heteroduplexes, or both.

scholarly journals Suppressor Analysis of the Saccharomyces cerevisiae Gene REC104 Reveals a Genetic Interaction With REC102

Genetics ◽  
1999 ◽  
Vol 151 (4) ◽  
pp. 1261-1272 ◽  
Author(s):  
Laura Salem ◽  
Natalie Walter ◽  
Robert Malone
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Meiotic Recombination ◽  
Null Allele ◽  
Genetic Interaction ◽  
In Vitro Mutagenesis ◽  
Conditional Mutations ◽  
Suppressor Analysis

Abstract REC104 is a gene required for the initiation of meiotic recombination in Saccharomyces cerevisiae. To better understand the role of REC104 in meiosis, we used an in vitro mutagenesis technique to create a set of temperature-conditional mutations in REC104 and used one ts allele (rec104-8) in a screen for highcopy suppressors. An increased dosage of the early exchange gene REC102 was found to suppress the conditional recombinational reduction in rec104-8 as well as in several other conditional rec104 alleles. However, no suppression was observed for a null allele of REC104, indicating that the suppression by REC102 is not “bypass” suppression. Overexpression of the early meiotic genes REC114, RAD50, HOP1, and RED1 fails to suppress any of the rec104 conditional alleles, indicating that the suppression might be specific to REC102.

scholarly journals Coupling DNA Replication and Spindle Function in Saccharomyces cerevisiae

Cells ◽  
2021 ◽  
Vol 10 (12) ◽  
pp. 3359
Author(s):  
Dimitris Liakopoulos
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Dna Replication ◽  
Molecular Mechanisms ◽  
Genome Duplication ◽  
Yeast Cells ◽  
Yeast Saccharomyces Cerevisiae ◽  
Spindle Dynamics ◽  
Eukaryotic Organisms ◽  
Spindle Function

In the yeast Saccharomyces cerevisiae DNA replication and spindle assembly can overlap. Therefore, signaling mechanisms modulate spindle dynamics in order to ensure correct timing of chromosome segregation relative to genome duplication, especially when replication is incomplete or the DNA becomes damaged. This review focuses on the molecular mechanisms that coordinate DNA replication and spindle dynamics, as well as on the role of spindle-dependent forces in DNA repair. Understanding the coupling between genome duplication and spindle function in yeast cells can provide important insights into similar processes operating in other eukaryotic organisms, including humans.

scholarly journals Dynamic Localization of Protein Phosphatase Type 1 in the Mitotic Cell Cycle of Saccharomyces cerevisiae

2000 ◽  
Vol 149 (1) ◽  
pp. 125-140 ◽  
Author(s):  
Andrew Bloecher ◽  
Kelly Tatchell
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Cell Cycle ◽  
Protein Phosphatase ◽  
Essential Gene ◽  
Mitotic Cell ◽  
Type I ◽  
Mitotic Cell Cycle ◽  
Dependent Manner ◽  
Bud Neck ◽  
Protein Phosphatase Type

Protein phosphatase type I (PP1), encoded by the single essential gene GLC7 in Saccharomyces cerevisiae, functions in diverse cellular processes. To identify in vivo subcellular location(s) where these processes take place, we used a functional green fluorescent protein (GFP)–Glc7p fusion protein. Time-lapse fluorescence microscopy revealed GFP–Glc7p localizes predominantly in the nucleus throughout the mitotic cell cycle, with the highest concentrations in the nucleolus. GFP–Glc7p was also observed in a ring at the bud neck, which was dependent upon functional septins. Supporting a role for Glc7p in bud site selection, a glc7-129 mutant displayed a random budding pattern. In α-factor treated cells, GFP–Glc7p was located at the base of mating projections, again in a septin-dependent manner. At the start of anaphase, GFP–Glc7p accumulated at the spindle pole bodies and remained there until cytokinesis. After anaphase, GFP–Glc7p became concentrated in a ring that colocalized with the actomyosin ring. A GFP–Glc7-129 fusion was defective in localizing to the bud neck and SPBs. Together, these results identify sites of Glc7p function and suggest Glc7p activity is regulated through dynamic changes in its location.

Yeast Mutants That Produce a Novel Type of Ascus Containing Asci Instead of Spores

Genetics ◽  
1996 ◽  
Vol 144 (3) ◽  
pp. 979-989 ◽  
Author(s):  
Zhixiong Xue ◽  
Xiaoyin Shan ◽  
Alex Sinelnikov ◽  
Teri Melese
Keyword(s):  
Cell Cycle ◽  
Essential Gene ◽  
Mitotic Cell ◽  
Yeast Cells ◽  
Mitotic Cell Cycle ◽  
Spindle Formation ◽  
Bud Formation ◽  
Yeast Mutants ◽  
Two Hybrid

Abstract Tetraploid yeast cells lacking BFR1 or overexpressing an essential gene BBPl produce a novel type of ascus that contains asci instead of spores. We show here that the asci within an ascus likely arise because a/α spores undergo a second round of meiosis. Cells depleted of Bbplp or lacking Bfr1p are defective in a number of processes such as nuclear segregation, bud formation, cytokinesis and nuclear spindle formation. Furthermore, deletion of BFR1 or overexpression of BBP1 leads to an increase in cell ploidy, indicating that Bfr1p and Bbplp play roles in both the mitotic cell cycle and meiosis. Bfr1p and Bbp1p interact with each other in a two hybrid assay, further suggesting that they might form a complex important for cell cycle coordination.

scholarly journals Yeast Ppz1 protein phosphatase toxicity involves the alteration of multiple cellular targets

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Diego Velázquez ◽  
Marcel Albacar ◽  
Chunyi Zhang ◽  
Carlos Calafí ◽  
María López-Malo ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Transcription Factor ◽  
Protein Phosphatase ◽  
Mitotic Cell ◽  
Yeast Cells ◽  
Growth Defect ◽  
Cellular Targets ◽  
Major Mechanism ◽  
Bud Emergence ◽  
Phosphorylation Pattern

Abstract Control of the protein phosphorylation status is a major mechanism for regulation of cellular processes, and its alteration often lead to functional disorders. Ppz1, a protein phosphatase only found in fungi, is the most toxic protein when overexpressed in Saccharomyces cerevisiae. To investigate the molecular basis of this phenomenon, we carried out combined genome-wide transcriptomic and phosphoproteomic analyses. We have found that Ppz1 overexpression causes major changes in gene expression, affecting ~ 20% of the genome, together with oxidative stress and increase in total adenylate pools. Concurrently, we observe changes in the phosphorylation pattern of near 400 proteins (mainly dephosphorylated), including many proteins involved in mitotic cell cycle and bud emergence, rapid dephosphorylation of Snf1 and its downstream transcription factor Mig1, and phosphorylation of Hog1 and its downstream transcription factor Sko1. Deletion of HOG1 attenuates the growth defect of Ppz1-overexpressing cells, while that of SKO1 aggravates it. Our results demonstrate that Ppz1 overexpression has a widespread impact in the yeast cells and reveals new aspects of the regulation of the cell cycle.

scholarly journals Mitochondrial Superoxide Dismutase and Yap1p Act as a Signaling Module Contributing to Ethanol Tolerance of the Yeast Saccharomyces cerevisiae

2016 ◽  
Vol 83 (3) ◽  
Author(s):  
Anna N. Zyrina ◽  
Ekaterina A. Smirnova ◽  
Olga V. Markova ◽  
Fedor F. Severin ◽  
Dmitry A. Knorre
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Hydrogen Peroxide ◽  
Superoxide Dismutase ◽  
Ethanol Tolerance ◽  
Yeast Cells ◽  
Ethanol Stress ◽  
Mitochondrial Enzymes ◽  
Mitochondrial Superoxide ◽  
Mitochondrial Superoxide Dismutase

ABSTRACT There are two superoxide dismutases in the yeast Saccharomyces cerevisiae—cytoplasmic and mitochondrial enzymes. Inactivation of the cytoplasmic enzyme, Sod1p, renders the cells sensitive to a variety of stresses, while inactivation of the mitochondrial isoform, Sod2p, typically has a weaker effect. One exception is ethanol-induced stress. Here we studied the role of Sod2p in ethanol tolerance of yeast. First, we found that repression of SOD2 prevents ethanol-induced relocalization of yeast hydrogen peroxide-sensing transcription factor Yap1p, one of the key stress resistance proteins. In agreement with this, the levels of Trx2p and Gsh1p, proteins encoded by Yap1 target genes, were decreased in the absence of Sod2p. Analysis of the ethanol sensitivities of the cells lacking Sod2p, Yap1p, or both indicated that the two proteins act in the same pathway. Moreover, preconditioning with hydrogen peroxide restored the ethanol resistance of yeast cells with repressed SOD2. Interestingly, we found that mitochondrion-to-nucleus signaling by Rtg proteins antagonizes Yap1p activation. Together, our data suggest that hydrogen peroxide produced by Sod2p activates Yap1p and thus plays a signaling role in ethanol tolerance. IMPORTANCE Baker's yeast harbors multiple systems that ensure tolerance to high concentrations of ethanol. Still, the role of mitochondria under severe ethanol stress in yeast is not completely clear. Our study revealed a signaling function of mitochondria which contributes significantly to the ethanol tolerance of yeast cells. We found that mitochondrial superoxide dismutase Sod2p and cytoplasmic hydrogen peroxide sensor Yap1p act together as a module of the mitochondrion-to-nucleus signaling pathway. We also report cross talk between this pathway and the conventional retrograde signaling cascade activated by dysfunctional mitochondria.

scholarly journals An auxin signaling network translates low-sugar-state input into compensated cell enlargement in the fugu5 cotyledon

PLoS Genetics ◽  
2021 ◽  
Vol 17 (8) ◽  
pp. e1009674
Author(s):  
Hiromitsu Tabeta ◽  
Shunsuke Watanabe ◽  
Keita Fukuda ◽  
Shizuka Gunji ◽  
Mariko Asaoka ◽  
...  
Keyword(s):  
Atpase Activity ◽  
Molecular Mechanisms ◽  
Genetic Interaction ◽  
Mitotic Cell ◽  
Fine Tuning ◽  
Auxin Signaling ◽  
Cell Enlargement ◽  
Loss Of Function ◽  
Nutrient Reserves

In plants, the effective mobilization of seed nutrient reserves is crucial during germination and for seedling establishment. The Arabidopsis H+-PPase-loss-of-function fugu5 mutants exhibit a reduced number of cells in the cotyledons. This leads to enhanced post-mitotic cell expansion, also known as compensated cell enlargement (CCE). While decreased cell numbers have been ascribed to reduced gluconeogenesis from triacylglycerol, the molecular mechanisms underlying CCE remain ill-known. Given the role of indole 3-butyric acid (IBA) in cotyledon development, and because CCE in fugu5 is specifically and completely cancelled by ech2, which shows defective IBA-to-indoleacetic acid (IAA) conversion, IBA has emerged as a potential regulator of CCE. Here, to further illuminate the regulatory role of IBA in CCE, we used a series of high-order mutants that harbored a specific defect in IBA-to-IAA conversion, IBA efflux, IAA signaling, or vacuolar type H+-ATPase (V-ATPase) activity and analyzed the genetic interaction with fugu5–1. We found that while CCE in fugu5 was promoted by IBA, defects in IBA-to-IAA conversion, IAA response, or the V-ATPase activity alone cancelled CCE. Consistently, endogenous IAA in fugu5 reached a level 2.2-fold higher than the WT in 1-week-old seedlings. Finally, the above findings were validated in icl–2, mls–2, pck1–2 and ibr10 mutants, in which CCE was triggered by low sugar contents. This provides a scenario in which following seed germination, the low-sugar-state triggers IAA synthesis, leading to CCE through the activation of the V-ATPase. These findings illustrate how fine-tuning cell and organ size regulation depend on interplays between metabolism and IAA levels in plants.

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