Mitochondria and male disease

  title={Mitochondria and male disease},
  author={Steven A. Frank and Laurence D. Hurst},
Mother’s curse and indirect genetic effects: Do males matter to mitochondrial genome evolution?
It is argued that mtIGEs are probably common, and that this might ameliorate or exacerbate mother's curse, and could plausibly allow the mitochondrial genome to evolve via kin selection.
Coadaptation of mitochondrial and nuclear genes, and the cost of mother's curse
A population genetic analysis of mito-nuclear coadaptation to resolve mother's curse effects shows that the magnitude of the ‘male mitochondrial load’—the negative impact of mitochondrial substitutions on male fitness components—may be large, even when genetic variation for compensatory evolution is abundant.
Effects of mitochondrial genomic variation on life history trait expression in Drosophila melanogaster
It is concluded that the present text is intended to serve as a guide for the development of a post-modern alternative to the traditional one-size-fits-all approach to distributive justice.
Mitonuclear Epistasis for Development Time and Its Modification by Diet in Drosophila
The results demonstrate thatMitonuclear epistases are context dependent, suggesting the selective pressure acting on mitonuclear genotypes may vary with food environment in a genotype-specific manner.
Can paternal leakage maintain sexually antagonistic polymorphism in the cytoplasm?
It is shown how paternal leakage can dampen the evolution of deleterious male effects associated with predominant maternal inheritance of cytoplasm, potentially explaining why ’mother's curse’ is less pervasive than predicted by earlier work.
The costs of being male: are there sex-specific effects of uniparental mitochondrial inheritance?
It is suggested that the existence of male expression-biased mtDNA mutations is likely to be a broad phenomenon, but that these mutations remain cryptic owing to the presence of counter-adapted nuclear compensatory modifier mutations, which offset their deleterious effects.
uniparental mitochondrial inheritance ? The costs of being male : are there sex-specific effects of
References This article cites 82 articles, 21 of which can be accessed free Subject collections (283 articles)
Mitochondrial haplotype does not influence sperm motility in a UK population of men.
Mitochondrial haplotype is unlikely to be a reliable genetic marker of male factor infertility and individual SNPs which were in linkage disequilibrium and dispersed across the mitochondrial genome, and therefore sensitive to mtDNA variation, were not predictive of sperm motility.
Mitochondrial haplotype does not affect sperm velocity in the zebra finch Taeniopygia guttata
Using quantitative genetic ‘animal’ models, there is no evidence that in this system mitochondrial mutations have asymmetric fitness effects on males and females, leading to genetic variation in male fertility that is blind to natural selection.
A comparison of nuclear and cytoplasmic genetic effects on sperm competitiveness and female remating in a seed beetle
It is found that sperm competitiveness and remating are primarily encoded by nuclear genes, and a male’s sperm competitiveness phenotype was contingent on an interaction between the competing male genotypes.


Mitochondrial deoxyribonucleic acid 4977-bp deletion is associated with diminished fertility and motility of human sperm.
The results reveal a negative correlation between sperm motility and the proportion of 4977-bp-deleted mtDNA and suggest that mtDNA mutations may play an important role in some pathophysiological conditions in human spermatozoa.
Multiple deletions of mtDNA in two brothers with sideroblastic anemia and mitochondrial myopathy and in their asymptomatic mother.
It is concluded that two brothers presented with a clinical picture characterized by sideroblastic anemia, mild pancreatic insufficiency and progressive muscle weakness suffer from a familial form of mitochondrial disease clinically resembling Pearson's syndrome, with a probably autosomal dominant inheritance.
Andrology: Mitochondrial disease and reduced sperm motility
Sperm motility was investigated in a patient with a mitochondrial disease caused by reduced activity of the mitochondrial enzyme complexes I and IV, and in two control subjects, indicating that mitochondrial dysfunction causes reduced sperm motility in some men.
Identical mitochondrial DNA deletion in mother with progressive external ophthalmoplegia and son with Pearson marrow-pancreas syndrome.
This case extends the clinical phenotype of the Pearson syndrome and raises the possibility that developmentally regulated tissue-specific nuclear factors are responsible for the differential phenotypic expression of these two mitochondrial disorders.
Reevaluation of the linkage of an optic atrophy susceptibility gene to X-chromosomal markers in Finnish families with Leber hereditary optic neuroretinopathy (LHON)
The results of this present study clearly demonstrate that the earlier close linkage to DXS7 is implausible, and the altered Z is due to revised pedigrees, the usemore of liability classes, and separation of the families according to the associated mtDNA mutation.
Diseases of the mitochondrial DNA.
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    Annual review of biochemistry
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The author reveals evidence for OXPHOS DEFECTS in COMMON DEGENERATIVE DISEASes in NUCLEAR-CYTOPLASMIC INTERACTIONS and provides evidence for the importance of knowing the carrier and removal status of canine coronavirus.
Metabolic regulation in mammalian sperm: mitochondrial volume determines sperm length and flagellar beat frequency.
Using data on the morphometric dimensions of over 200 mammalian species, it is found that an allometric relationship exists between midpiece length and flagellum length, implying that, at least in mammals, the mechanisms for energy production and dissipation in sperm flagella are highly conserved.
Optic atrophy in Leber hereditary optic neuroretinopathy is probably determined by an X-chromosomal gene closely linked to DXS7.
No evidence of heterogeneity was found among different types of families, with or without a known mtDNA mutation associated with LHON, and genetic linkage of the liability to develop optic atrophy to 15 polymorphic markers on the X chromosome was studied.