scholarly journals Plasticity of Mitochondrial DNA Inheritance and its Impact on Nuclear Gene Transcription in Yeast Hybrids

2020 ◽  
Vol 8 (4) ◽  
pp. 494 ◽  
Author(s):  
Sarah K. Hewitt ◽  
Kobchai Duangrattanalert ◽  
Tim Burgis ◽  
Leo A.H. Zeef ◽  
Samina Naseeb ◽  
...  
Keyword(s):  
Mitochondrial Dna ◽  
Yeast Species ◽  
Hybrid Cell ◽  
Nuclear Gene ◽  
Cellular Functions ◽  
Hybrid Fitness ◽  
Rich Media ◽  
Hybrid Genome ◽  
Allele Type ◽  
Respiratory Conditions

Mitochondrial DNA (mtDNA) in yeast is biparentally inherited, but colonies rapidly lose one type of parental mtDNA, thus becoming homoplasmic. Therefore, hybrids between the yeast species possess two homologous nuclear genomes, but only one type of mitochondrial DNA. We hypothesise that the choice of mtDNA retention is influenced by its contribution to hybrid fitness in different environments, and the allelic expression of the two nuclear sub-genomes is affected by the presence of different mtDNAs in hybrids. Saccharomyces cerevisiae/S. uvarum hybrids preferentially retained S. uvarum mtDNA when formed on rich media at colder temperatures, while S. cerevisiae mtDNA was primarily retained on non-fermentable carbon source, at any temperature. Transcriptome data for hybrids harbouring different mtDNA showed a strong environmentally dependent allele preference, which was more important in respiratory conditions. Co-expression analysis for specific biological functions revealed a clear pattern of concerted allelic transcription within the same allele type, which supports the notion that the hybrid cell works preferentially with one set of parental alleles (or the other) for different cellular functions. Given that the type of mtDNA retained in hybrids affects both nuclear expression and fitness, it might play a role in driving hybrid genome evolution in terms of gene retention and loss.

scholarly journals Plasticity of Mitochondrial DNA Inheritance and its Impact on Nuclear Gene Transcription in Yeast Hybrids

2018 ◽  
Author(s):  
Sarah K. Hewitt ◽  
Kobchai Duangrattanalert ◽  
Tim Burgis ◽  
Leo A.H. Zeef ◽  
Daniela Delneri
Keyword(s):  
Mitochondrial Dna ◽  
Expression Profiles ◽  
Hybrid Cell ◽  
Carbon Sources ◽  
Nuclear Genome ◽  
Nuclear Gene ◽  
The Other ◽  
Cellular Functions ◽  
Hybrid Fitness ◽  
Selection Of

AbstractMitochondrial DNA (mtDNA) in budding yeast is biparentally inherited, but colonies rapidly lose one type of parental mtDNA, becoming homoplasmic. Therefore, hybrids between different yeast species possess two homologous nuclear genomes, but only one type of mitochondrial DNA. We hypothesise that the choice of mtDNA retention is influenced by its contribution to hybrid fitness in different environments, and that the allelic expression of the two nuclear sub-genomes is affected by the presence of different mtDNAs in hybrids. Here, we crossedSaccharomyces cerevisiaewithS. uvarumunder different environmental conditions and examined the plasticity of the retention of mtDNA in each hybrid. We showed that on fermentable carbon sources at warm temperatures each parental mtDNA was equally likely to be retained, while at colder temperatures, hybrids preferentially retained mtDNA derived fromS. uvarum. On a non-fermentable carbon source, hybrids retainedS. cerevisiaemtDNA, independent of temperature. By acquiring transcriptome data and co-expression profiles for hybrids harbouring different mtDNA in a selection of environments, we found a clear pattern of concerted allelic transcription of one or the other sub-genome for specific biological pathways, supporting the notion that the hybrid cell works preferentially with one set of parental alleles or the other according to specific cellular functions. We argue that the type of mtDNA retained in hybrids affects the expression of the nuclear genome and the organism fitness in different environments, and therefore may have a role in driving the evolution of the hybrid nuclear genome in terms of gene retention and loss.

scholarly journals Recombining Your Way Out of Trouble: The Genetic Architecture of Hybrid Fitness under Environmental Stress

2019 ◽  
Vol 37 (1) ◽  
pp. 167-182 ◽  
Author(s):  
Zebin Zhang ◽  
Devin P Bendixsen ◽  
Thijs Janzen ◽  
Arne W Nolte ◽  
Duncan Greig ◽  
...  
Keyword(s):  
Environmental Stress ◽  
Evolutionary Potential ◽  
Genetic Trait ◽  
Hybrid Fitness ◽  
Mixed Effect ◽  
Mixed Effect Models ◽  
Hybrid Genome ◽  
Chromosome Associations ◽  
Low Coverage ◽  
Negative Epistasis

Abstract Hybridization between species can either promote or impede adaptation. But we know very little about the genetic basis of hybrid fitness, especially in nondomesticated organisms, and when populations are facing environmental stress. We made genetically variable F2 hybrid populations from two divergent Saccharomyces yeast species. We exposed populations to ten toxins and sequenced the most resilient hybrids on low coverage using ddRADseq to investigate four aspects of their genomes: 1) hybridity, 2) interspecific heterozygosity, 3) epistasis (positive or negative associations between nonhomologous chromosomes), and 4) ploidy. We used linear mixed-effect models and simulations to measure to which extent hybrid genome composition was contingent on the environment. Genomes grown in different environments varied in every aspect of hybridness measured, revealing strong genotype–environment interactions. We also found selection against heterozygosity or directional selection for one of the parental alleles, with larger fitness of genomes carrying more homozygous allelic combinations in an otherwise hybrid genomic background. In addition, individual chromosomes and chromosomal interactions showed significant species biases and pervasive aneuploidies. Against our expectations, we observed multiple beneficial, opposite-species chromosome associations, confirmed by epistasis- and selection-free computer simulations, which is surprising given the large divergence of parental genomes (∼15%). Together, these results suggest that successful, stress-resilient hybrid genomes can be assembled from the best features of both parents without paying high costs of negative epistasis. This illustrates the importance of measuring genetic trait architecture in an environmental context when determining the evolutionary potential of genetically diverse hybrid populations.

A human mitochondrial transcriptional activator can functionally replace a yeast mitochondrial HMG-box protein both in vivo and in vitro

1993 ◽  
Vol 13 (3) ◽  
pp. 1951-1961
Author(s):  
M A Parisi ◽  
B Xu ◽  
D A Clayton
Keyword(s):  
Transcription Factor ◽  
Mitochondrial Dna ◽  
Nuclear Gene ◽  
Transcriptional Activator ◽  
Yeast Mitochondria ◽  
Yeast Protein ◽  
Mitochondrial Transcription ◽  
Mitochondrial Transcription Factor ◽  
Mitochondrial Transcription Factor A

Human mitochondrial transcription factor A is a 25-kDa protein that binds immediately upstream of the two major mitochondrial promoters, thereby leading to correct and efficient initiation of transcription. Although the nature of yeast mitochondrial promoters is significantly different from that of human promoters, a potential functional homolog of the human transcriptional activator protein has been previously identified in yeast mitochondria. The importance of the yeast protein in yeast mitochondrial DNA function has been shown by inactivation of its nuclear gene (ABF2) in Saccharomyces cerevisiae cells resulting in loss of mitochondrial DNA. We report here that the nuclear gene for human mitochondrial transcription factor A can be stably expressed in yeast cells devoid of the yeast homolog protein. The human protein is imported efficiently into yeast mitochondria, is processed correctly, and rescues the loss-of-mitochondrial DNA phenotype in a yeast abf2 strain, thus functionally substituting for the yeast protein. Both human and yeast proteins affect yeast mitochondrial transcription initiation in vitro, suggesting that the two proteins may have a common role in this fundamental process.

scholarly journals The Typically Mitochondrial DNA-encoded ATP6 Subunit of the F1F0-ATPase Is Encoded by a Nuclear Gene inChlamydomonas reinhardtii

2001 ◽  
Vol 277 (8) ◽  
pp. 6051-6058 ◽  
Author(s):  
Soledad Funes ◽  
Edgar Davidson ◽  
M. Gonzalo Claros ◽  
Robert van Lis ◽  
Xochitl Pérez-Martı́nez ◽  
...  
Keyword(s):  
Mitochondrial Dna ◽  
Nuclear Gene ◽  
F1f0 Atpase

scholarly journals Mitochondrial DNA as an inflammatory mediator in cardiovascular diseases

2018 ◽  
Vol 475 (5) ◽  
pp. 839-852 ◽  
Author(s):  
Hiroyuki Nakayama ◽  
Kinya Otsu
Keyword(s):  
Mitochondrial Dna ◽  
Inflammatory Responses ◽  
Inflammatory Cells ◽  
Nuclear Factor Κb ◽  
Sterile Inflammation ◽  
Microbial Infection ◽  
Cellular Functions ◽  
Radical Oxygen Species ◽  
Cardiac Inflammation ◽  
Contraction And Relaxation

Mitochondria play a central role in multiple cellular functions, including energy production, calcium homeostasis, and cell death. Currently, growing evidence indicates the vital roles of mitochondria in triggering and maintaining inflammation. Chronic inflammation without microbial infection — termed sterile inflammation — is strongly involved in the development of heart failure. Sterile inflammation is triggered by the activation of pattern recognition receptors (PRRs) that sense endogenous ligands called damage-associated molecular patterns (DAMPs). Mitochondria release multiple DAMPs including mitochondrial DNA, peptides, and lipids, which induce inflammation via the stimulation of multiple PRRs. Among the mitochondrial DAMPs, mitochondrial DNA (mtDNA) is currently highlighted as the DAMP that mediates the activation of multiple PRRs, including Toll-like receptor 9, Nod-like receptors, and cyclic GMP–AMP synthetase/stimulator of interferon gene pathways. These PRR signalling pathways, in turn, lead to the activation of nuclear factor-κB and interferon regulatory factor, which enhances the transcriptional activity of inflammatory cytokines and interferons, and induces the recruitment of inflammatory cells. As the heart is an organ comprising abundant mitochondria for its ATP consumption (needed to maintain constant cyclic contraction and relaxation), the generation of massive amounts of mitochondrial radical oxygen species and mitochondrial DAMPs are predicted to occur and promote cardiac inflammation. Here, we will focus on the role of mtDNA in cardiac inflammation and review the mechanism and pathological significance of mtDNA-induced inflammatory responses in cardiac diseases.

Detection of two cryptic taxa in Meristogenys amoropalamus (Amphibia, Ranidae) through nuclear and mitochondrial DNA analyses

Zootaxa ◽  
2008 ◽  
Vol 1843 (1) ◽  
pp. 24 ◽  
Author(s):  
TOMOHIKO SHIMADA ◽  
MASAFUMI MATSUI ◽  
PAUL YAMBUN ◽  
MAKLARIN LAKIM ◽  
MARYATI MOHAMED
Keyword(s):  
Mitochondrial Dna ◽  
Nuclear Gene ◽  
Single Species ◽  
Sympatric Species ◽  
12S Rrna ◽  
Dna Analyses ◽  
Deep Coalescence ◽  
Pomc Gene ◽  
Cryptic Taxa ◽  
Rag 1

We identified three distinct sympatric lineages of frogs among specimens previously considered a single species (Meris- togenys amoropalamus Matsui), based on 909 bp of mitochondrial DNA (12S rRNA and cytochrome b). To seek evidence of reproductive isolation between these lineages, we first analyzed a 249-bp fragment of the nuclear proopiomelanocortin (POMC) gene and found five haplotypes, of which two were limited to lineage 1 and three belonged to lineages 3 and 4. In a subsequent phylogenetic analysis of a 1313-bp fragment of nuclear POMC, Rag-1, and rhodopsin, lineage 1 was again distinct, while lineages 3 and 4 could not be differentiated. The results of the nuclear gene analyses suggest that lineage 1 is strongly isolated reproductively from lineages 3 and 4, which are not isolated from each other. This conclusion conforms to groupings based on larval morphology. These results indicate that frogs morphologically identified as M. amoropalamus should be split into two sympatric species, one of which contains two mitochondrial lineages that have presumably been retained via deep coalescence.

scholarly journals Respiration-Dependent Utilization of Sugars in Yeasts: a Determinant Role for Sugar Transporters

2002 ◽  
Vol 184 (2) ◽  
pp. 427-432 ◽  
Author(s):  
Paola Goffrini ◽  
Iliana Ferrero ◽  
Claudia Donnini
Keyword(s):  
Yeast Species ◽  
Kluyveromyces Lactis ◽  
Sugar Uptake ◽  
Sugar Transporters ◽  
High Substrate ◽  
Fermentative Growth ◽  
Major Bottleneck ◽  
Respiratory Conditions

ABSTRACT In many yeast species, including Kluyveromyces lactis, growth on certain sugars (such as galactose, raffinose, and maltose) occurs only under respiratory conditions. If respiration is blocked by inhibitors, mutation, or anaerobiosis, growth does not take place. This apparent dependence on respiration for the utilization of certain sugars has often been suspected to be associated with the mechanism of the sugar uptake step. We hypothesized that in many yeast species, the permease activities for these sugars are not sufficient to ensure the high substrate flow that is necessary for fermentative growth. By introducing additional sugar permease genes, we have obtained K. lactis strains that were capable of growing on galactose and raffinose in the absence of respiration. High dosages of both the permease and maltase genes were indeed necessary for K. lactis cells to grow on maltose in the absence of respiration. These results strongly suggest that the sugar uptake step is the major bottleneck in the fermentative assimilation of certain sugars in K. lactis and probably in many other yeasts.

PET112, a Saccharomyces cerevisiae nuclear gene required to maintain rho + mitochondrial DNA

1994 ◽  
Vol 25 (4) ◽  
pp. 299-304 ◽  
Author(s):  
Julio J. Mulero ◽  
Janet K. Rosenthal ◽  
Thomas D. Fox
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Mitochondrial Dna ◽  
Nuclear Gene

199 EVIDENCE FOR A NOVEL PERTURBATION IN CLONED FETUSES: MITOCHONDRIAL DNA DEPLETION

2007 ◽  
Vol 19 (1) ◽  
pp. 216
Author(s):  
S. Hiendleder ◽  
D. Bebbere ◽  
S. E. Ulbrich ◽  
V. Zakhartchenko ◽  
M. Weppert ◽  
...  
Keyword(s):  
Mitochondrial Dna ◽  
Real Time ◽  
Nuclear Gene ◽  
Complement C3 ◽  
Mtdna Copy Number ◽  
Vitro Fertilization ◽  
Mitochondrial Transcription Factor ◽  
Mitochondrial Dna Depletion

The reported mtDNA turnover and plasticity of mtDNA copy number in mammalian zygotes and early embryos (McConnel and Petrie 2004 Reprod. Biomed. Online 9, 418–424) have revealed a potential for adverse effects of in vitro embryo techniques on mtDNA and mitochondrial function. We explored the effects of in vitro fertilization (IVF) and somatic cell nuclear transfer cloning (NT) on relative mtDNA amount and phenotype in viable bovine fetuses recovered 80 days after the initiation of embryonic development (Hiendleder et al. 2004 Biol. Reprod. 71, 217–223). We sampled brain, liver, and skeletal muscle to represent all 3 embryonic germ layers, and compared IVF-fetuses (n = 24), NT-fetuses (n = 23), and fetuses generated by in vivo insemination (controls, n = 24). This experimental approach allowed us to distinguish abnormalities specific to cloning from more general consequences of in vitro embryo manipulation. We analyzed relative mtDNA amounts by real-time quantitative PCR (qPCR) and amplified a segment of the mtDNA control region that was normalized against the nuclear gene complement C3. ANOVA (SPSS 13.0) of qPCR data and phenotypic parameters revealed significant effects of fetus group on mtDNA amount in liver (P < 0.05) and muscle (P < 0.01), and on fetus (P < 0.001), heart (P < 0.001), and liver (P < 0.001) weights. The mtDNA amount in all tissues from IVF-fetuses was normal, but mtDNA levels in liver (-23%; P < 0.05) and muscle (-24%; P < 0.01) of NT-fetuses were significantly lower than in controls. Fetuses derived from IVF- or NT-embryos were similar in weight and displayed fetal overgrowth (+19% and +22%; P < 0.001), but only the NT-fetuses were affected by disproportionate hepatomegaly and cardiomegaly with 31% and 49% increases (ANCOVA; P < 0.001) in their respective organ weights. This further partitioned NT-fetuses from IVF-fetuses and identified symptoms that are also encountered in mitochondrial DNA depletion syndromes (MDDS): a phenotypically heterogeneous group of human disorders characterized by loss of mtDNA from various tissues during development and associated respiratory chain dysfunction. The MDDS phenotypes have mainly been classified into a hepatocerebral (MIM 251880) or myopathic (MIM 609560) form, and neonates and infants display a spectrum of abnormalities, including hepatomegaly and cardiomegaly, that are similar or identical to phenotypic abnormalities commonly encountered in cloned mammals. Reduced mtDNA amounts in NT-fetuses could stem from perturbation of mtDNA during the reported turnover period, or be a secondary effect of epigenetic change in nuclear-encoded genes involved in mtDNA replication and stability. Mitochondrial transcription factor A (TFAM) is regulated by CpG methylation in vitro, but our real-time RT-PCR quantification of TFAM transcript in liver and muscle of a subset of NT- and control fetuses failed to detect significant differences (P > 0.10). In conclusion, our observed reduction of mtDNA amount in cloned fetuses provides the molecular basis for a mitochondrial perspective on pathological phenotypes of cloned mammals, and may explain similarities to mitochondrial disease in human.

The role of the Mpv17 protein mutations of which cause mitochondrial DNA depletion syndrome (MDDS): lessons from homologs in different species

2015 ◽  
Vol 396 (1) ◽  
pp. 13-25 ◽  
Author(s):  
Stefanie Löllgen ◽  
Hans Weiher
Keyword(s):  
Mitochondrial Dna ◽  
Tricarboxylic Acid Cycle ◽  
Clinical Manifestations ◽  
Nuclear Gene ◽  
Genotoxic Stress ◽  
Strand Break ◽  
Temperature Sensitive ◽  
Inner Mitochondrial Membrane ◽  
Knock Out ◽  
Mitochondrial Dna Depletion

Abstract Mitochondrial DNA depletion syndromes (MDDS) are severe pediatric diseases with diverse clinical manifestations. Gene mutations that underlie MDDS have been associated with alterations in the mitochondrial DNA (mtDNA) replication machinery or in mitochondrial deoxyribonucleoside triphosphate pools. However, the nuclear gene MPV17, whose mutated forms are associated with hepatocerebral MDDS in humans, plays a so-far unknown role in mtDNA maintenance. A high degree of conservation has been determined between MPV17 and its mouse (Mpv17), zebrafish (tra) and yeast (SYM1) homologs, respectively, whereby mutants in these cause very different phenotypes. While dysfunction in this gene in humans causes fatal liver disease, kidney pathology is induced in mice. Moreover, in zebrafish inactivation of the Mpv17 homolog was detected as a viable dyscolouration mutant. Knock out of the yeast ortholog results in a temperature-sensitive metabolic growth phenotype. Detailed analyses on common denominators between these different phenotypes strengthen the hypothesis that the Mpv17 protein forms a channel in the inner mitochondrial membrane, allowing small molecules – in vertebrates probably nucleotides, and in yeast probably intermediates of the tricarboxylic acid cycle – to pass. Moreover, a function modifying the pathologic manifestations of MPV17-related disease in mice has been identified. This signaling pathway remarkably involves the non-mitochondrial catalytic subunit of DNA-dependent protein kinase (PRKDC), important in double-strand break repair resistance against reactive oxygen-induced genotoxic stress.

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