Evidence of Introgressive Hybridization in the Genus Stizostedion: Interspecific Transfer of Mitochondrial DNA between Sauger and Walleye

1988 ◽  
Vol 45 (11) ◽  
pp. 2035-2041 ◽  
Author(s):  
Neil Billington ◽  
Paul D. N. Hebert ◽  
Robert D. Ward
Keyword(s):  
Mitochondrial Dna ◽  
Mitochondrial Genome ◽  
Introgressive Hybridization ◽  
Stizostedion Vitreum ◽  
Stizostedion Canadense ◽  
Lake Simcoe ◽  
Allozyme Loci ◽  
Interspecific Transfer

The mitochondrial genotypes of walleye (Stizostedion vitreum) and sauger (Stizostedion canadense) are readily differentiated, permitting an analysis of the incidence of hybridization between the taxa. We provide evidence that introgression of sauger into walleye has occurred: two female walleye collected from Lake Simcoe contained a mitochondrial genome identical to that of sauger. Not only were these two fish morphologically indistinguishable from typical walleye, they were homozygous for the diagnostic alleles characteristic of walleye at the Mdh-3 and Pgm-1 allozyme loci. Sauger have not been recorded in Lake Simcoe, but a few individuals may have been inadvertently introduced during stocking programs and introgressed with walleye due to a lack of conspecific mates.

Comparison of Allozyme and Mitochondrial DNA Variation in Populations of Walleye, Stizostedion vitreum

1989 ◽  
Vol 46 (12) ◽  
pp. 2074-2084 ◽  
Author(s):  
Robert D. Ward ◽  
Neil Billington ◽  
Paul D. N. Hebert
Keyword(s):  
Mitochondrial Dna ◽  
Glacial Refugia ◽  
Divergence Times ◽  
Stizostedion Vitreum ◽  
Dna Variation ◽  
Mtdna Variation ◽  
Mtdna Haplotypes ◽  
Total Genetic Diversity ◽  
Allozyme Loci ◽  
Organelle Genes

Twelve populations of walleye (Stizostedion vitreum) from the Great Lakes and three populations from northern Manitoba were screened for allozyme and mitochondrial DNA (mtDNA) variation. Nine enzyme loci known to show genetic variation were screened in all fish: five of them (Prot-4, Prot-2, Mdh-3, Idh-1, Adh) showed appreciable polymorphism. MtDNA was examined in all fish using six endonucleases that detected polymorphic sites and a further 13 endonucleases that detected only monomorphic sites. Only one of the allozyme loci (Prot-4) showed evidence of geographic patterning of allele frequencies. By contrast, the mtDNA haplotypes showed clear geographic variation. The proportion of total genetic diversity attributable to population differentiation (Gst) was three to five times greater for mtDNA than for the allozymes. Gst values for organelle genes are expected on theoretical grounds to be greater than for nuclear genes, and this expected difference may be enhanced in walleye because of the likelihood that, in this species, male-mediated gene flow exceeds that of females. The distributions of mtDNA haplotypes and estimated divergence times are consistent with the derivation of extant walleye populations from three different glacial refugia.

scholarly journals Mitochondrial DNA Methylation and Human Diseases

2021 ◽  
Vol 22 (9) ◽  
pp. 4594
Author(s):  
Andrea Stoccoro ◽  
Fabio Coppedè
Keyword(s):  
Dna Methylation ◽  
Mitochondrial Dna ◽  
Mitochondrial Genome ◽  
Nuclear Dna ◽  
Epigenetic Modification ◽  
Nuclear Genome ◽  
Epigenetic Modifications ◽  
Human Diseases ◽  
Loop Region ◽  
D Loop

Epigenetic modifications of the nuclear genome, including DNA methylation, histone modifications and non-coding RNA post-transcriptional regulation, are increasingly being involved in the pathogenesis of several human diseases. Recent evidence suggests that also epigenetic modifications of the mitochondrial genome could contribute to the etiology of human diseases. In particular, altered methylation and hydroxymethylation levels of mitochondrial DNA (mtDNA) have been found in animal models and in human tissues from patients affected by cancer, obesity, diabetes and cardiovascular and neurodegenerative diseases. Moreover, environmental factors, as well as nuclear DNA genetic variants, have been found to impair mtDNA methylation patterns. Some authors failed to find DNA methylation marks in the mitochondrial genome, suggesting that it is unlikely that this epigenetic modification plays any role in the control of the mitochondrial function. On the other hand, several other studies successfully identified the presence of mtDNA methylation, particularly in the mitochondrial displacement loop (D-loop) region, relating it to changes in both mtDNA gene transcription and mitochondrial replication. Overall, investigations performed until now suggest that methylation and hydroxymethylation marks are present in the mtDNA genome, albeit at lower levels compared to those detectable in nuclear DNA, potentially contributing to the mitochondria impairment underlying several human diseases.

scholarly journals Reduced Variation in Drosophila simulans Mitochondrial DNA

Genetics ◽  
1996 ◽  
Vol 144 (4) ◽  
pp. 1519-1528
Author(s):  
J William O Ballad ◽  
Joy Hatzidakis ◽  
Timothy L Karr ◽  
Martin Kreitman
Keyword(s):  
Mitochondrial Dna ◽  
Mitochondrial Genome ◽  
Evolutionary Dynamics ◽  
Selective Sweep ◽  
Mitochondrial Gene ◽  
Drosophila Simulans ◽  
Dramatic Reduction ◽  
Nucleotide Variability ◽  
Pooled Samples ◽  
Mitochondrial Gene Mutation

We investigated the evolutionary dynamics of infection of a Drosophila simulans population by a maternally inherited insect bacterial parasite, Wolbachia, by analyzing nucleotide variability in three regions of the mitochondrial genome in four infected and 35 uninfected lines. Mitochondrial variability is significantly reduced compared to a noncoding region of a nuclear-encoded gene in both uninfected and pooled samples of flies, indicating a sweep of genetic variation. The selective sweep of mitochondrial DNA may have been generated by the fixation of an advantageous mitochondrial gene mutation in the mitochondrial genome. Alternatively, the dramatic reduction in mitochondrial diversity may be related to Wolbachia.

scholarly journals Mitochondrial DNA Toxicity in Forebrain Neurons Causes Apoptosis, Neurodegeneration, and Impaired Behavior

2010 ◽  
Vol 30 (6) ◽  
pp. 1357-1367 ◽  
Author(s):  
Knut H. Lauritzen ◽  
Olve Moldestad ◽  
Lars Eide ◽  
Harald Carlsen ◽  
Gaute Nesse ◽  
...  
Keyword(s):  
Mitochondrial Dna ◽  
Mitochondrial Genome ◽  
Cognitive Abilities ◽  
Natural Aging ◽  
Base Substitution ◽  
Behavioral Alterations ◽  
Adult Mice ◽  
Progressive Loss ◽  
Forebrain Neurons ◽  
High Level

ABSTRACT Mitochondrial dysfunction underlying changes in neurodegenerative diseases is often associated with apoptosis and a progressive loss of neurons, and damage to the mitochondrial genome is proposed to be involved in such pathologies. In the present study we designed a mouse model that allows us to specifically induce mitochondrial DNA toxicity in the forebrain neurons of adult mice. This is achieved by CaMKIIα-regulated inducible expression of a mutated version of the mitochondrial UNG DNA repair enzyme (mutUNG1). This enzyme is capable of removing thymine from the mitochondrial genome. We demonstrate that a continual generation of apyrimidinic sites causes apoptosis and neuronal death. These defects are associated with behavioral alterations characterized by increased locomotor activity, impaired cognitive abilities, and lack of anxietylike responses. In summary, whereas mitochondrial base substitution and deletions previously have been shown to correlate with premature and natural aging, respectively, we show that a high level of apyrimidinic sites lead to mitochondrial DNA cytotoxicity, which causes apoptosis, followed by neurodegeneration.

scholarly journals Whole mitochondrial genome screening in maternally inherited non-syndromic hearing impairment using a microarray resequencing mitochondrial DNA chip

2007 ◽  
Vol 15 (11) ◽  
pp. 1145-1155 ◽  
Author(s):  
Marianne Lévêque ◽  
Sandrine Marlin ◽  
Laurence Jonard ◽  
Vincent Procaccio ◽  
Pascal Reynier ◽  
...  
Keyword(s):  
Mitochondrial Dna ◽  
Mitochondrial Genome ◽  
Hearing Impairment ◽  
Dna Chip ◽  
Genome Screening ◽  
Syndromic Hearing Impairment

scholarly journals Mitochondrial DNA polymorphism and cardiovascular continuum diseases

2018 ◽  
pp. 9-13
Author(s):  
М.В. Голубенко ◽  
Р.Р. Салахов ◽  
Т.В. Шумакова ◽  
С.В. Буйкин ◽  
О.А. Макеева ◽  
...  
Keyword(s):  
Mitochondrial Dna ◽  
Cardiovascular Diseases ◽  
Mitochondrial Genome ◽  
Dna Polymorphism ◽  
Nuclear Genome ◽  
Published Data ◽  
Human Populations ◽  
Mitochondrial Dna Polymorphism ◽  
Polymorphism Level ◽  
Cardiovascular Continuum

Митохондриальный геном кодирует жизненно важные белки субъединиц дыхательной цепи и характеризуется высоким уровнем полиморфизма в популяциях человека. Однако работы по поиску генов предрасположенности к многофакторным заболеваниям, в том числе сердечно-сосудистым, часто ограничиваются анализом ядерного генома. В то же время показано, что отдельные генотипы мтДНК могут отличаться более высокой или низкой эффективностью окислительного фосфорилирования. Выявлены ассоциации популяционного полиморфизма мтДНК с сердечно-сосудистыми заболеваниями. Согласно результатам наших исследований, а также опубликованных другими авторами результатам ассоциативных и функциональных исследований, можно говорить о том, что эффект полиморфизма мтДНК проявляется чаще не в предрасположенности к сердечно-сосудистым заболеваниям в целом, а в риске развития осложнений и коморбидных фенотипов в пределах синтропии сердечно-сосудистого континуума. Mitochondrial genome, encoding respiratory chain subunits, is characterized by high polymorphism level in human populations. In most studies for susceptibility genes for common diseases, including cardiovascular diseases, the analysis is limited to the nuclear genome. It was shown that particular mtDNA genotypes may differ by oxidative phosphorylation efficiency. Some associations of mtDNA polymorphisms with cardiovascular diseases have been found. According to our results and published data, we suggest that mtDNA effect on cardiovascular system does not manifest in predisposition to cardiovascular diseases themselves but rather in risk of complications and comorbidities in the cardiovascular continuum.

Mitochondrial cardiovascular diseases

2020 ◽  
pp. 325-342
Author(s):  
Perry Elliott ◽  
Pier D. Lambiase ◽  
Dhavendra Kumar
Keyword(s):  
Mitochondrial Dna ◽  
Hypertrophic Cardiomyopathy ◽  
Cardiovascular Diseases ◽  
Mitochondrial Genome ◽  
Mitochondrial Disease ◽  
Clinical Management ◽  
Cardiac Involvement ◽  
Mitochondrial Disorders ◽  
Barth Syndrome

This chapter begins by defining the mitochondrial genome, and the subsequent assessment of suspected mitochondrial DNA (mtDNA) disorders. The incidence and prevalence of cardiac involvement in mitochondrial disorders is covered, including the probably under-reporting of this. Different cardiovascular phenotypes associated with mitochondrial disease (arrhythmias, hypertrophic cardiomyopathy, Barth syndrome etc.) are all described, and then the clinical management of the diseases are explained. As there is no fixed treatment, pharmacological regimens to avoid, and other approaches are also included.

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