Deficiencies in mitochondrial DNA compromise the survival of yeast cells at critically high temperatures

Abstract

To address possible roles of mitochondrial genes in adaptation of eukaryotic cells to critical temperatures, we compared thermotolerance of mitochondrial rho mutants and wild type cells of six rho positive yeast species: Candida glabrata, Saccharomyces bayanus, Saccharomyces cerevisiae, Saccharomyces eubayanus, Saccharomyces paradoxus and Saccharomyces pastorianus. All rho mutants manifested compromised thermotolerance as a common phenotype. Analysis of viabilities at critical temperatures (32-45 °C) showed the reduction of maximum permissive temperatures (MPTs) in all rho mutants in comparison to their wild type counterparts. Degrees of the compromised thermotolerance depended on maximum permissive temperatures for wild type cells: the highest levels of MPT reductions for rho mutants took place in species and strains with highest MPTs for wild types. Short term exposures of S. cerevisiae cells (up to 3.5h) at non-permissive temperatures (45 °C and 50 °C) also lead to more rapid cell death of rho mutants as compared to wild type cells. We conclude that: (1) compromised thermotolerance could be a generic phenotypic property of rho mutants; (2) the enhanced thermotolerance of cells possessing mitochondrial genomes could be one of selective advantages in adaptation to environmental factors, in particular to enhanced temperatures.

Mitochondria-encoded genes contribute to the evolution of heat and cold tolerance amongSaccharomycesspecies

“…Has adaptation played a role in driving these incompatibilities? Although no direct links are proven, evolution of the mitochondrial genome and mito-nuclear epistasis has been linked to multiple phenotypes (Solieri et al 2008;Albertin et al 2013;Picazo et al 2014), including 37°C growth (Paliwal et al 2014, Wolters et al 2018, Leducq et al 2017, and deficiencies in mitochondrial DNA cause heat sensitivity (Zubko and Zubko 2014). Here, we show that mtDNA is important for evolution of heat and cold tolerance in distantly related species, caused by the accumulation of multiple small-to-medium effect changes and potentially mito-nuclear epistasis.…”

Mitochondria-encoded genes contribute to evolution of heat and cold tolerance in yeast

“…Has adaptation played a role in driving these incompatibilities? Although no direct links are proven, evolution of the mitochondrial genome and mitonuclear epistasis has been linked to multiple phenotypes ( 21 , 37 , 38 ), including 37°C growth ( 16 – 18 ), and deficiencies in mtDNA cause heat sensitivity ( 39 ). Here, we show that mtDNA is important for evolution of heat and cold tolerance in distantly related species, caused by the accumulation of multiple small-to-medium effect changes and potentially mitonuclear epistasis.…”

Messenger RNAs of Yeast Virus-Like Elements Contain Non-templated 5′ Poly(A) Leaders, and Their Expression Is Independent of eIF4E and Pab1

“…Pab1 is a physiological stress sensor that rapidly localizes to stress granules upon stress insult (Riback et al, 2017). Others have also shown that deficiencies in mitochondrial DNA decrease yeast tolerance to heat stress (Zubko and Zubko, 2014). We can speculate that the elevated temperature and stress induced by non-functional eIF4E could lead to the sequestration and decreased availability of Pab1 and thus to higher translatability and, consequently, stability of the toxin-coding uncapped and 5′ polyadenylated K1ORF2 mRNAs.…”