New mitochondrial genome organization in three interspecific somatic hybrids of Medicago sativa including the parent-specific amplification of substoichiometric mitochondrial DNA units

2001 ◽  
Vol 103 (6-7) ◽  
pp. 972-978 ◽  
Author(s):  
F. Pupilli ◽  
P. Labombarda ◽  
S. Arcioni
Keyword(s):  
Mitochondrial Dna ◽  
Mitochondrial Genome ◽  
Medicago Sativa ◽  
Genome Organization ◽  
Somatic Hybrids ◽  
Specific Amplification ◽  
Interspecific Somatic Hybrids

Mitochondrial genome diversity and the evolution of mitochondrial DNA

1982 ◽  
Vol 60 (3) ◽  
pp. 157-171 ◽  
Author(s):  
Michael W. Gray
Keyword(s):  
Mitochondrial Dna ◽  
Mitochondrial Genome ◽  
Comparative Studies ◽  
Genome Organization ◽  
Sequence Divergence ◽  
Genome Diversity ◽  
Primary Sequence ◽  
Mitochondrial Ribosomes ◽  
Intergenic Sequences ◽  
Mitochondrial Genome Diversity

Mitochondrial DNA (mtDNA) is functionally conservative, encoding basically the same genes in all eukaryotes, yet mitochondrial genome organization and expression show an amazing diversity, and mtDNAs are highly variable in size and in potential information content. This review focuses on certain novel features of mitochondrial genome diversity which have emerged from recent comparative studies of mtDNA and which indicate that, in the course of evolution, mtDNAs have undergone massive sequence rearrangements, have lost (and (or) acquired) large stretches of sequence between and within genes, and have sustained, in at least some cases, an unusually high degree of primary sequence divergence. It is suggested that much of the mitochondrial genome diversity that presently exists can be accounted for by a variable (and in some cases, quite rapid) rate of evolution of mtDNA. An endosymbiotic origin of mitochondria can be accommodated in this scenario if it is assumed that the "protomitochondrion," although eubacterial in essential elements of its translation system (e.g., ribosomal RNA), was unlike modern eubacteria in containing introns and extensive intergenic "spacer" sequences in its genome. Differing evolutionary pressures on the "free-living" and "intracellular" progenitors of eubacteria and mitochondria, respectively, could have resulted in the subsequent elimination of these "extra" sequences at different rates and to different extents, leading in the case of humans and other mammals to a mitochondrial genome having little or no noncoding sequences. Viewed from this perspective, most of the introns and intergenic sequences in some larger mtDNAs are considered to be retained primitive traits, vestiges of genome organization in the universal "progenote" from which a very early divergence of the eukaryotic nuclear, eubacterial, and archaebacterial lineages has been postulated. In all but the more conservative mitochondrial genomes, rapid primary sequence divergence will have tended to obscure the phylogenetic ancestry of most mtDNA-encoded macromolecules. This could explain why animal and fungal mitochondrial tRNAs, and plant mitochondrial 5S rRNA, are not typically eubacterial. A variable rate of mtDNA evolution is indicated by the fact that plant mitochondrial ribosomes are less "atypical" than the same components in other mitochondria, with plant (wheat) mitochondrial small-subunit rRNA showing much clearer indications of a eubacterial origin than its counterparts in animal (human, mouse) and fungal (yeast) mitochondrial ribosomes. Thus, the plant mitochondrial genome may be evolving considerably less rapidly than its counterparts in fungi and (especially) vertebrate animals. Our present state of knowledge about the structure, function, and evolution of mtDNA demonstrates both the power of, and essential need for, broadly based comparative studies in this field.

scholarly journals Frequent tRNA gene translocation towards the boundaries with control regions contributes to the highly dynamic mitochondrial genome organization of the parasitic lice of mammals

BMC Genomics ◽  
2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Wen-Ge Dong ◽  
Yalun Dong ◽  
Xian-Guo Guo ◽  
Renfu Shao
Keyword(s):  
Mitochondrial Genome ◽  
Control Region ◽  
Genome Organization ◽  
Trna Gene ◽  
Trna Genes ◽  
Single Chromosome ◽  
Gene Translocation ◽  
Sucking Lice ◽  
Different Types ◽  
Mt Genome

Abstract Background The typical single-chromosome mitochondrial (mt) genome of animals has fragmented into multiple minichromosomes in the lineage Mitodivisia, which contains most of the parasitic lice of eutherian mammals. These parasitic lice differ from each other even among congeneric species in mt karyotype, i.e. the number of minichromosomes, and the gene content and gene order in each minichromosome, which is in stark contrast to the extremely conserved single-chromosome mt genomes across most animal lineages. How fragmented mt genomes evolved is still poorly understood. We use Polyplax sucking lice as a model to investigate how tRNA gene translocation shapes the dynamic mt karyotypes. Results We sequenced the full mt genome of the Asian grey shrew louse, Polyplax reclinata. We then inferred the ancestral mt karyotype for Polyplax lice and compared it with the mt karyotypes of the three Polyplax species sequenced to date. We found that tRNA genes were entirely responsible for mt karyotype variation among these three species of Polyplax lice. Furthermore, tRNA gene translocation observed in Polyplax lice was only between different types of minichromosomes and towards the boundaries with the control region. A similar pattern of tRNA gene translocation can also been seen in other sucking lice with fragmented mt genomes. Conclusions We conclude that inter-minichromosomal tRNA gene translocation orientated towards the boundaries with the control region is a major contributing factor to the highly dynamic mitochondrial genome organization in the parasitic lice of mammals.

The mitochondrial genome organization of a maize fertile cmsT revertant line is generated through recombination between two sets of repeats.

Genetics ◽  
1990 ◽  
Vol 124 (2) ◽  
pp. 423-428 ◽  
Author(s):  
C M Fauron ◽  
M Havlik ◽  
R I Brettell
Keyword(s):  
Mitochondrial Genome ◽  
Genome Organization ◽  
Callus Tissue ◽  
Mitochondrial Genomes ◽  
Normal Type ◽  
Male Sterile ◽  
Sequence Complexity ◽  
Mtdna Organization ◽  
Callus Tissue Culture ◽  
Fertile Revertant

Abstract The mitochondrial genome (mtDNA) organization from a fertile revertant line (V3) derived from the maize cytoplasmic male sterile type T (cmsT) callus tissue culture has been determined. We report that the sequence complexity can be mapped on to a circular "master chromosome" of 705 kb which includes a duplication of 165 kb of DNA when compared to its male sterile progenitor. Associated with this event is also a 0.423-kb deletion, which removed the cmsT-associated urf13 gene. As found for the maize normal type (N) and cmsT mitochondrial genomes, the V3 master chromosome also exists as a multipartite structure generated by recombination through repeated sequences.

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.

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