Mitochondrial DNA and the evolutionary genetics of higher animals

1986 ◽  
Vol 312 (1154) ◽  
pp. 325-342 ◽  
Keyword(s):  
Mitochondrial Dna ◽  
Population Genetic ◽  
Life Histories ◽  
Nuclear Dna ◽  
Molecular Level ◽  
Evolutionary Genetics ◽  
Genetic System ◽  
Phylogenetic Status ◽  
First Time ◽  
Genetic Characters

Mitochondrial DNA (mtDNA) in higher animals is rapidly becoming a well characterized genetic system at the molecular level. In this paper, I shift the focus to consider questions in organismal evolution that can be addressed by mtDNA assay. For the first time, it is possible to estimate empirically matriarchal phylogeny; to determine directionality in crosses producing hybrids; and to study the population genetic consequences of varying female demographies and life histories. The data obtainable from mtDNA may be especially well suited for studies of population genetic structure, dispersal, and historical zoogeography. The female-mediated, clonal transmission of mtDNA is also stimulating new ways of thinking about times to common ancestry of asexual lineages within otherwise sexually reproducing populations; about the possible relevance of mtDNA-nuclear DNA interactions to reproductive isolation; and about the very meaning of the phylogenetic status of related species with respect to particular kinds of genetic characters. These and other topics are reviewed.

scholarly journals Mitochondrial DNA: a blind spot in neuroepigenetics

2012 ◽  
Vol 3 (2) ◽  
pp. 107-115 ◽  
Author(s):  
Hari Manev ◽  
Svetlana Dzitoyeva ◽  
Hu Chen
Keyword(s):  
Mitochondrial Dna ◽  
Nuclear Dna ◽  
Blind Spot ◽  
Dna Methyltransferases ◽  
Molecular Neuroscience ◽  
Dna Modifications ◽  
System Physiology ◽  
Near Future ◽  
First Time ◽  
The Brain

AbstractNeuroepigenetics, which includes nuclear DNA modifications, such as 5-methylcytosine and 5-hydroxymethylcytosine and modifications of nuclear proteins, such as histones, is emerging as the leading field in molecular neuroscience. Historically, a functional role for epigenetic mechanisms, including in neuroepigenetics, has been sought in the area of the regulation of nuclear transcription. However, one important compartment of mammalian cell DNA, different from nuclear DNA but equally important for physiological and pathological processes (including in the brain), mitochondrial DNA has for the most part not had a systematic epigenetic characterization. The importance of mitochondria and mitochondrial DNA (particularly its mutations) in central nervous system physiology and pathology has long been recognized. Only recently have the mechanisms of mitochondrial DNA methylation and hydroxymethylation, including the discovery of mitochondrial DNA-methyltransferases and the presence and functionality of 5-methylcytosine and 5-hydroxymethylcytosine in mitochondrial DNA (e.g., in modifying the transcription of mitochondrial genome), been unequivocally recognized as a part of mammalian mitochondrial physiology. Here, we summarize for the first time evidence supporting the existence of these mechanisms and propose the term ‘mitochondrial epigenetics’ to be used when referring to them. Currently, neuroepigenetics does not include mitochondrial epigenetics – a gap that we expect to close in the near future.

scholarly journals Genetic research of anadromous herring in Volga-Caspian fishery basin

2019 ◽  
Vol 2019 (4) ◽  
pp. 116-123
Author(s):  
Ekaterina Grigorievna Makarova ◽  
Natalia Victorovna Kozlova ◽  
Margarita Armenovna Baregamyan ◽  
Tatyana Victorovna Voinova
Keyword(s):  
Mitochondrial Dna ◽  
Cytochrome B ◽  
Nuclear Dna ◽  
Molecular Genetic ◽  
Genetic Research ◽  
Nucleotide Substitutions ◽  
Polymorphic Loci ◽  
Low Level ◽  
Dna Microsatellite ◽  
First Time

For the first time, a study of genetic variability of Caspian anadromous herring was carried out using molecular genetic methods. Sequencing of the cytochrome B site of mitochondrial DNA allowed to identify 7 haplotypes. The most massive haplotype was Hap_Alosa1 noted in 29 herring individuals. Five minor haplotypes were detected in few fish individuals. In the marine period of life in fish caught in the Northern Caspian there were noted rare haplotypes Hap_Alosa6 and Hap_Alosa7. In the river period of life in the Volga herring there was observed Hap_Alosa5. The revealed polymorphism of haplotypes was represented by single nucleotide substitutions. The genetic analysis of migratory herring does not give grounds for isolating the studied fish into separate groups. The marked low level of nucleotide diversity of cytochrome B gene of mitochondrial DNA of the anodromous herring indicates a significant genetic homogeneity of the species within the studied range. The results of analysis of nuclear DNA microsatellite loci showed that only three of the six sites of the studied gene were polymorphic. In individuals caught in the river period of life, only Af20 (out of the 6 loci studied) was polymorphic and was characterized by 4 alleles. In a sample of herring from the Northern Caspian, 3 polymorphic loci (Aa16, Af6 and Af20) were observed, in which 2 alleles were recorded. The observed heterozygosity varied from 0.313 to 0.667 exceeding the level of expected heterozygosity. In polymorphic loci a deficit of heterozygotes was not noted. The results obtained in this study indicate a low level of genetic variation of anadromous herring.

scholarly journals The Role of Mitochondria in Carcinogenesis

2021 ◽  
Vol 22 (10) ◽  
pp. 5100
Author(s):  
Paulina Kozakiewicz ◽  
Ludmiła Grzybowska-Szatkowska ◽  
Marzanna Ciesielka ◽  
Jolanta Rzymowska
Keyword(s):  
Prostate Cancer ◽  
Mitochondrial Dna ◽  
Nuclear Dna ◽  
Dna Polymorphisms ◽  
Gene Encoding ◽  
Dna Mutations ◽  
Nadh Ubiquinone Oxidoreductase ◽  
Gene Coi ◽  
The Impact

The mitochondria are essential for normal cell functioning. Changes in mitochondrial DNA (mtDNA) may affect the occurrence of some chronic diseases and cancer. This process is complex and not entirely understood. The assignment to a particular mitochondrial haplogroup may be a factor that either contributes to cancer development or reduces its likelihood. Mutations in mtDNA occurring via an increase in reactive oxygen species may favour the occurrence of further changes both in mitochondrial and nuclear DNA. Mitochondrial DNA mutations in postmitotic cells are not inherited, but may play a role both in initiation and progression of cancer. One of the first discovered polymorphisms associated with cancer was in the gene NADH-ubiquinone oxidoreductase chain 3 (mt-ND3) and it was typical of haplogroup N. In prostate cancer, these mutations and polymorphisms involve a gene encoding subunit I of respiratory complex IV cytochrome c oxidase subunit 1 gene (COI). At present, a growing number of studies also address the impact of mtDNA polymorphisms on prognosis in cancer patients. Some of the mitochondrial DNA polymorphisms occur in both chronic disease and cancer, for instance polymorphism G5913A characteristic of prostate cancer and hypertension.

scholarly journals Evaluation of the Variability of the ORF34, ORF68, and MLST Genes in EHV-1 from South Korea

Pathogens ◽  
2021 ◽  
Vol 10 (4) ◽  
pp. 425
Author(s):  
Hyung-Woo Kang ◽  
Eun-Yong Lee ◽  
Kyoung-Ki Lee ◽  
Mi-Kyeong Ko ◽  
Ji-Young Park ◽  
...  
Keyword(s):  
Nucleotide Sequence ◽  
South Korea ◽  
Molecular Level ◽  
Economic Losses ◽  
Equine Herpesvirus ◽  
Equine Herpesvirus 1 ◽  
Mlst Analysis ◽  
Herpesvirus 1 ◽  
First Time ◽  
Group 1

Equine herpesvirus-1 (EHV-1) is an important pathogen in horses. It affects horses worldwide and causes substantial economic losses. In this study, for the first time, we characterized EHV-1 isolates from South Korea at the molecular level. We then aimed to determine the genetic divergences of these isolates by comparing them to sequences in databases. In total, 338 horse samples were collected, and 12 EHV-1 were isolated. We performed ORF30, ORF33, ORF68, and ORF34 genetic analysis and carried out multi-locus sequence typing (MLST) of 12 isolated EHV-1. All isolated viruses were confirmed as non-neuropathogenic type, showing N752 of ORF30 and highly conserved ORF33 (99.7–100%). Isolates were unclassified using ORF68 analysis because of a 118 bp deletion in nucleotide sequence 701–818. Seven EHV-1 isolates (16Q4, 19R166-1, 19R166-6, 19/10/15-2, 19/10/15-4, 19/10/18-2, 19/10/22-1) belonged to group 1, clade 10, based on ORF34 and MLST analysis. The remaining 5 EHV-1 isolates (15Q25-1, 15D59, 16Q5, 16Q40, 18D99) belonged to group 7, clade 6, based on ORF34 and MLST analysis.

Evidence for genetic hybridization between Ixodes scapularis and Ixodes cookei

2017 ◽  
Vol 95 (8) ◽  
pp. 527-537 ◽  
Author(s):  
James W. Patterson ◽  
Anna M. Duncan ◽  
Kelsey C. McIntyre ◽  
Vett K. Lloyd
Keyword(s):  
Mitochondrial Dna ◽  
Genetic Analysis ◽  
New Brunswick ◽  
Nuclear Dna ◽  
Ixodes Scapularis ◽  
Companion Animals ◽  
Genetic Introgression ◽  
Eastern Canada ◽  
As Species ◽  
Intermediate Traits

Ixodes scapularis Say, 1821 (the black-legged tick) is becoming established in Canada. The northwards expansion of I. scapularis leads to contact between I. scapularis and Ixodes cookei Packard, 1869, a well-established tick species in Eastern Canada. Examination of I. cookei and I. scapularis collected from New Brunswick revealed ticks with ambiguous morphologies, with either a mixture or intermediate traits typical of I. scapularis and I. cookei, including in characteristics typically used as species identifiers. Genetic analysis to determine if these ticks represent hybrids revealed that four had I. cookei derived mitochondrial DNA but I. scapularis nuclear DNA. In one case, the nuclear sequence showed evidence of heterozygosity for I. scapularis and I. cookei sequences, whereas in the others, the nuclear DNA appeared to be entirely derived from I. scapularis. These data strongly suggest genetic hybridization between these two species. Ixodes cookei and hybrid ticks were readily collected from humans and companion animals and specimens infected with Borrelia burgdorferi Johnson et al., 1984, the causative agent of Lyme disease, were identified. These findings raise the issue of genetic introgression of I. scapularis genes into I. cookei and warrant reassessment of the capacity of I. cookei and I. cookei × I. scapularis hybrids to vector Borrelia infection.

scholarly journals Mitochondrial DNA Heteroplasmy as an Informational Reservoir Dynamically Linked to Metabolic and Immunological Processes Associated with COVID-19 Neurological Disorders

2021 ◽  
Author(s):  
George B. Stefano ◽  
Richard M. Kream
Keyword(s):  
Mitochondrial Dna ◽  
Mitochondrial Function ◽  
Neurological Disorders ◽  
Nuclear Dna ◽  
Mitochondrial Dynamics ◽  
Cell Types ◽  
Tissue Specific ◽  
Copy Numbers ◽  
The Central Nervous System ◽  
Mitochondrial Dna Heteroplasmy

AbstractMitochondrial DNA (mtDNA) heteroplasmy is the dynamically determined co-expression of wild type (WT) inherited polymorphisms and collective time-dependent somatic mutations within individual mtDNA genomes. The temporal expression and distribution of cell-specific and tissue-specific mtDNA heteroplasmy in healthy individuals may be functionally associated with intracellular mitochondrial signaling pathways and nuclear DNA gene expression. The maintenance of endogenously regulated tissue-specific copy numbers of heteroplasmic mtDNA may represent a sensitive biomarker of homeostasis of mitochondrial dynamics, metabolic integrity, and immune competence. Myeloid cells, monocytes, macrophages, and antigen-presenting dendritic cells undergo programmed changes in mitochondrial metabolism according to innate and adaptive immunological processes. In the central nervous system (CNS), the polarization of activated microglial cells is dependent on strategically programmed changes in mitochondrial function. Therefore, variations in heteroplasmic mtDNA copy numbers may have functional consequences in metabolically competent mitochondria in innate and adaptive immune processes involving the CNS. Recently, altered mitochondrial function has been demonstrated in the progression of coronavirus disease 2019 (COVID-19) due to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. Accordingly, our review is organized to present convergent lines of empirical evidence that potentially link expression of mtDNA heteroplasmy by functionally interactive CNS cell types to the extent and severity of acute and chronic post-COVID-19 neurological disorders.

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.

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