Genetic evidence for different RAD52-dependent intrachromosomal recombination pathways in Saccharomyces cerevisiae

1995 ◽  
Vol 27 (4) ◽  
pp. 298-305 ◽  
Author(s):  
Andr�s Aguilera
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Genetic Evidence ◽  
Intrachromosomal Recombination

scholarly journals Loss of Ubp3 increases silencing, decreases unequal recombination in rDNA, and shortens the replicative life span in Saccharomyces cerevisiae

2014 ◽  
Vol 25 (12) ◽  
pp. 1916-1924 ◽  
Author(s):  
David Öling ◽  
Rehan Masoom ◽  
Kristian Kvint
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Rna Polymerase ◽  
Life Span ◽  
Rna Polymerase Ii ◽  
Ribosomal Dna ◽  
Genetic Evidence ◽  
Wild Type ◽  
Replicative Life Span ◽  
Unequal Recombination

Ubp3 is a conserved ubiquitin protease that acts as an antisilencing factor in MAT and telomeric regions. Here we show that ubp3∆ mutants also display increased silencing in ribosomal DNA (rDNA). Consistent with this, RNA polymerase II occupancy is lower in cells lacking Ubp3 than in wild-type cells in all heterochromatic regions. Moreover, in a ubp3∆ mutant, unequal recombination in rDNA is highly suppressed. We present genetic evidence that this effect on rDNA recombination, but not silencing, is entirely dependent on the silencing factor Sir2. Further, ubp3∆ sir2∆ mutants age prematurely at the same rate as sir2∆ mutants. Thus our data suggest that recombination negatively influences replicative life span more so than silencing. However, in ubp3∆ mutants, recombination is not a prerequisite for aging, since cells lacking Ubp3 have a shorter life span than isogenic wild-type cells. We discuss the data in view of different models on how silencing and unequal recombination affect replicative life span and the role of Ubp3 in these processes.

Interchromosomal and intrachromosomal recombination in rad 18 mutants of Saccharomyces cerevisiae

1990 ◽  
Vol 222 (1) ◽  
pp. 25-32 ◽  
Author(s):  
Robert H. Schiestl ◽  
R. Daniel Gietz ◽  
P. J. Hastings ◽  
Ulrike Wintersberger
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Intrachromosomal Recombination

Genetic Evidence for a Morphogenetic Function of the Saccharomyces cerevisiae Pho85 Cyclin-Dependent Kinase

Genetics ◽  
2001 ◽  
Vol 157 (1) ◽  
pp. 39-51 ◽  
Author(s):  
Marc E Lenburg ◽  
Erin K O’Shea
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Genetic Evidence ◽  
Cyclin Dependent Kinase ◽  
G1 Cyclins ◽  
Novel Gene

Abstract The Saccharomyces cerevisiae PHO85 gene encodes a nonessential cyclin-dependent kinase that associates with 10 cyclin subunits. To survey the functions provided by Pho85, we identified mutants that require PHO85 for viability. We identified mutations that define seven Pho Eighty-Five Requiring or Efr loci, six of which are previously identified genes—BEM2 (YER155C), SPT7 (YBR081C), GCR1 (YPL075W), SRB5 (YGR104C), HFI1 (YPL254W), and BCK1 (YJL095W)—with one novel gene (YMR212C). We found that mutations in the EFR genes involved in morphogenesis are specifically inviable when the Pho85-associated G1 cyclins encoded by PCL1 and PCL2 are absent. pcl1Δ bem2, pcl1Δ pcl2Δ cla4Δ, and pcl1Δ pcl2Δ cdc42-1 strains are inviable. pcl1Δ pcl2Δ mpk1Δ, pcl1Δ pcl2Δ bck1, and pcl1Δ pcl2Δ cln1Δ cln2Δ strains are also inviable, but are rescued by osmotic stabilization with 1 m sorbitol. We propose that the G1 cyclins encoded by PCL1 and PCL2 positively regulate CDC42 or another morphogenesis promoting function.

scholarly journals Modification of a Ubiquitin-like Protein Paz2 Conducted Micropexophagy through Formation of a Novel Membrane Structure

2004 ◽  
Vol 15 (1) ◽  
pp. 58-70 ◽  
Author(s):  
Hiroyuki Mukaiyama ◽  
Misuzu Baba ◽  
Masako Osumi ◽  
Satoshi Aoyagi ◽  
Nobuo Kato ◽  
...  
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Pichia Pastoris ◽  
Membrane Structure ◽  
De Novo ◽  
Genetic Evidence ◽  
Membrane Formation ◽  
Modification System ◽  
Yeast Pichia Pastoris ◽  
Lysosomal Membranes ◽  
To Receive

Microautophagy is a versatile process in which vacuolar or lysosomal membranes directly sequester cytosolic targets for degradation. Recent genetic evidence suggested that microautophagy uses molecular machineries essential for macroautophagy, but the details of this process are still unknown. In this study, a ubiquitin-like protein Paz2 essential for micropexophagy in the yeast Pichia pastoris has been shown to receive modification through the function of Paz8 and Gsa7, yielding a modified form Paz2-I, similar to the ubiquitin-like lipidation of Aut7 that is essential for macroautophagy in Saccharomyces cerevisiae. We identified a novel membrane structure formed after the onset of micropexophagy, which we suggest is necessary for the sequestration of peroxisomes by the vacuole. Assembly of this newly formed membrane structure, which is followed by localization of Paz2 to it, was found to require a properly functioning Paz2-modification system. We herein show that Paz2 and its modification system conduct micropexophagy through formation of the membrane structure, which explains the convergence between micropexophagy and macroautophagy with regard to de novo membrane formation.

GENETIC EVIDENCE FOR 'DARWINIAN' SELECTION AT THE MOLECULAR LEVEL. I. THE EFFECT OF THE SUPPRESSIVE FACTOR ON CYTOPLASMICALLY-INHERITED ERYTHROMYCIN-RESISTANCE IN SACCHAROMYCES CEREVISIAE

1970 ◽  
Vol 12 (1) ◽  
pp. 129-136 ◽  
Author(s):  
Gerald H. Rank
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Mitochondrial Dna ◽  
Molecular Level ◽  
Genetic Evidence ◽  
Erythromycin Resistance ◽  
Darwinian Selection ◽  
Level I

A study of the suppressive factor of Saccharomyces cerevisiae and its effects on the transmission of cytoplasmically-inherited erythromycin resistance showed that loss of erythromycin resistance was contingent on suppressitivity, and that strains carrying the suppressive factor continuously segregated progeny cells that lacked resistance. It was suggested that suppressitivity is due to the presence, in suppressive strains, of rapidly-replicating abnormal mitochondrial DNA, and that loss of erythromycin resistance (coded for by normal mitochondrial DNA) is due to the replicative superiority of abnormal mitochondrial DNA.

scholarly journals Bypassing the Catalytic Activity of SIR2 for SIR Protein Spreading in Saccharomyces cerevisiae

2006 ◽  
Vol 17 (12) ◽  
pp. 5287-5297 ◽  
Author(s):  
Bo Yang ◽  
Ann L. Kirchmaier
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Catalytic Activity ◽  
Histone Deacetylase ◽  
Genetic Evidence ◽  
Enzymatic Function ◽  
Lysine Residues ◽  
Histone Hypoacetylation ◽  
In Cells

Sir protein spreading along chromosomes and silencing in Saccharomyces cerevisiae requires the NAD+-dependent histone deacetylase activity of Sir2p. We tested whether this requirement could be bypassed at the HM loci and telomeres in cells containing a stably expressed, but catalytically inactive mutant of Sir2p, sir2-345p, plus histone mutants that mimic the hypoacetylated state normally created by Sir2p. Sir protein spreading was rescued in sir2-345 mutants expressing histones in which key lysine residues in their N-termini had been mutated to arginine. Mating in these mutants was also partially restored upon overexpression of Sir3p. Together, these results indicate that histone hypoacetylation is sufficient for Sir protein spreading in the absence of production of 2′-O-acetyl-ADP ribose by sir2p and Sir2p's enzymatic function for silencing can be bypassed in a subset of cells in a given population. These results also provide genetic evidence for the existence of additional critical substrates of Sir2p for silencing in vivo.

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