scholarly journals Influence of mitochondrial DNA loss on the development of complex structured colonies of SK1 strains of yeast Saccharomyces cerevisiae

2018 ◽  
Vol 22 ◽  
pp. 68-73
Author(s):  
O. V. Pronina ◽  
S. R. Rushkovsky ◽  
B. V. Morgun ◽  
S. V. Demidov

Aim. Determine the effect of mitochondrial DNA loss on the formation of complex yeast colonies of Saccharomyces cerevisiae. Methods. Development of giant colonies of the parent strain SK1 (rho+) and the "petit" strain SK1p, which lost mtDNA (rho0 mutation), was observed for 40 days,. To find out zones of cell death in colonies, both strains were cultured on solid YPD media containing dyes that accumulate in dead cells. The survival of the cells within colony was estimated by the ability to create microcolonies.  Results. The loss of mitochondrial DNA in SK1p cells led to a decrease in colony area and to simplification of colony morphology on the YPD medium. When SK1p colonies were cultivated on media with addition of dyes, bright spot was formed in the center due to the dyes accumulation  in dead cells. At the same time, parent strain developed a uniform insignificant coloration.  Conclusions. rho0 mutation in SK1p yeast strain Saccharomyces cerevisiae led to a significant simplification of complex colony structure that formed on the nutrient medium YPD. The mitochondrial DNA loss in strain SK1p results in an accelerated cell death in the center of colony on YPD.Keywords: Saccharomyces cerevisiae, rho0, colonies, cell survival.

Genetics ◽  
2002 ◽  
Vol 162 (3) ◽  
pp. 1147-1156 ◽  
Author(s):  
Theodor Hanekamp ◽  
Mary K Thorsness ◽  
Indrani Rebbapragada ◽  
Elizabeth M Fisher ◽  
Corrine Seebart ◽  
...  

Abstract In the yeast Saccharomyces cerevisiae, certain mutant alleles of YME4, YME6, and MDM10 cause an increased rate of mitochondrial DNA migration to the nucleus, carbon-source-dependent alterations in mitochondrial morphology, and increased rates of mitochondrial DNA loss. While single mutants grow on media requiring mitochondrial respiration, any pairwise combination of these mutations causes a respiratory-deficient phenotype. This double-mutant phenotype allowed cloning of YME6, which is identical to MMM1 and encodes an outer mitochondrial membrane protein essential for maintaining normal mitochondrial morphology. Yeast strains bearing null mutations of MMM1 have altered mitochondrial morphology and a slow growth rate on all carbon sources and quantitatively lack mitochondrial DNA. Extragenic suppressors of MMM1 deletion mutants partially restore mitochondrial morphology to the wild-type state and have a corresponding increase in growth rate and mitochondrial DNA stability. A dominant suppressor also suppresses the phenotypes caused by a point mutation in MMM1, as well as by specific mutations in YME4 and MDM10.


2017 ◽  
Vol 200 (1) ◽  
pp. 33-46 ◽  
Author(s):  
Maria M. Bayliak ◽  
Olha V. Hrynkiv ◽  
Roksolana V. Knyhynytska ◽  
Volodymyr I. Lushchak

Genetics ◽  
2000 ◽  
Vol 154 (1) ◽  
pp. 147-154 ◽  
Author(s):  
Douglas J Kominsky ◽  
Peter E Thorsness

Abstract Organisms that can grow without mitochondrial DNA are referred to as “petite-positive” and those that are inviable in the absence of mitochondrial DNA are termed “petite-negative.” The petite-positive yeast Saccharomyces cerevisiae can be converted to a petite-negative yeast by inactivation of Yme1p, an ATP- and metal-dependent protease associated with the inner mitochondrial membrane. Suppression of this yme1 phenotype can occur by virtue of dominant mutations in the α- and γ-subunits of mitochondrial ATP synthase. These mutations are similar or identical to those occurring in the same subunits of the same enzyme that converts the petite-negative yeast Kluyveromyces lactis to petite-positive. Expression of YME1 in the petite-negative yeast Schizosaccharomyces pombe converts this yeast to petite-positive. No sequence closely related to YME1 was found by DNA-blot hybridization to S. pombe or K. lactis genomic DNA, and no antigenically related proteins were found in mitochondrial extracts of S. pombe probed with antisera directed against Yme1p. Mutations that block the formation of the F1 component of mitochondrial ATP synthase are also petite-negative. Thus, the F1 complex has an essential activity in cells lacking mitochondrial DNA and Yme1p can mediate that activity, even in heterologous systems.


2005 ◽  
Vol 33 (6) ◽  
pp. 1447-1450 ◽  
Author(s):  
M.A. Macris ◽  
P. Sung

Homologous recombination (HR) is a major pathway for the elimination of DNA DSBs (double-strand breaks) induced by high-energy radiation and chemicals, or that arise due to endogenous damage and stalled DNA replication forks. If not processed properly, DSBs can lead to cell death, chromosome aberrations and tumorigenesis. Even though HR is important for genome maintenance, it can also interfere with other DNA repair mechanisms and cause gross chromosome rearrangements. In addition, HR can generate DNA or nucleoprotein intermediates that elicit prolonged cell-cycle arrest and sometimes cell death. Genetic analyses in the yeast Saccharomyces cerevisiae have revealed a central role of the Srs2 helicase in preventing untimely HR events and in inhibiting the formation of potentially deleterious DNA structures or nucleoprotein complexes upon DNA replication stress. Paradoxically, efficient repair of DNA DSBs by HR is dependent on Srs2. In this paper, we review recent molecular studies aimed at deciphering the multifaceted role of Srs2 in HR and other cellular processes. These studies have provided critical insights into how HR is regulated in order to preserve genomic integrity and promote cell survival.


1993 ◽  
Vol 13 (5) ◽  
pp. 2697-2705
Author(s):  
R H Schiestl ◽  
M Dominska ◽  
T D Petes

When the yeast Saccharomyces cerevisiae was transformed with DNA that shares no homology to the genome, three classes of transformants were obtained. In the most common class, the DNA was inserted as the result of a reaction that appears to require base pairing between the target sequence and the terminal few base pairs of the transforming DNA fragment. In the second class, no such homology was detected, and the transforming DNA was integrated next to a CTT or GTT in the target; it is likely that these integration events were mediated by topoisomerase I. The final class involved the in vivo ligation of transforming DNA with nucleus-localized linear fragments of mitochondrial DNA.


2021 ◽  
Author(s):  
Victoria Bidiuk ◽  
Alexander Alexandrov ◽  
Airat Valiakhmetov

Abstract Extracellular pH has a significant impact on the physiology of the yeast cell, but its role in cell death has not been thoroughly investigated. We studied the effect of extracellular pH on the development of primary necrosis in Saccharomyces cerevisiae yeast under two general conditions leading to cell death. The first is sugar induced cell death (SICD), and the second is death caused by several specific gene deletions, which have been recently identified in a systematic screen. It was shown that in both cases, primary necrosis is suppressed at neutral pH. SICD was also inhibited by the protonophore dinitrophenol (DNP) and 150 mM extracellular K+, with the latter condition also benefiting survival of cell dying due to gene mutations. Thus, we show that neutral pH can suppress different types of primary necrosis. We suggest that changes to the cellular membrane potential can play a central role in yeast cell death.


2018 ◽  
Vol 9 ◽  
Author(s):  
Cédric Grangeteau ◽  
Florine Lepinois ◽  
Pascale Winckler ◽  
Jean-Marie Perrier-Cornet ◽  
Sebastien Dupont ◽  
...  

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