scholarly journals BIPARENTAL INHERITANCE OF MITOCHONDRIAL DNA IN RHESUS MACAQUES

2020 ◽  
Vol 114 (3) ◽  
pp. e433
Author(s):  
Hong Ma ◽  
Hayley Darby ◽  
Crystal Van Dyken ◽  
Aleksei Mikhalchenko ◽  
Nuria Marti-Gutierrez ◽  
...  
2006 ◽  
Vol 18 (2) ◽  
pp. 173
Author(s):  
T. Gibson ◽  
T. Quebedeaux ◽  
S. Rajasekaran ◽  
C. Brenner

Mitochondria are the most abundant organelles in mammalian oocytes and early embryos. Previous data have shown that mitochondrial DNA (mtDNA) deletions are present both in human oocytes and in embryos from in vitro fertilization (IVF) patients and suggest that accumulation of these deletions may contribute to mitochondrial dysfunction and impaired ATP production. In addition, high levels of mitochondrial mutations are present in skeletal muscle fibers from aged rhesus macaques. The specific aims of this study were to determine whether the mitochondrial common deletion is present in non-human primate oocytes and embryos generated by IVF and to determine whether mtDNA mutations are already present in immature oocytes from rhesus ovaries. Using a nested primer polymerase chain reaction (PCR) strategy, we determined the frequency of the rhesus common deletion in immature oocytes compared with stimulated oocytes and embryos. There was a low incidence (21%) of the rhesus common deletion present in immature, unstimulated oocytes derived from necropsied ovaries of 2 to 10-yr-old rhesus macaques. However, there was >3-fold increase (71.4%) in the frequency of deleted mtDNA in stimulated oocytes and IVF embryos from age-matched fertile monkeys. We postulated that, in addition to skeletal muscle, a similar time-dependent accumulation of mtDNA deletions occurs in fertile rhesus macaque oocytes and embryos. We are now investigating the effects of culture and passage number on mtDNA deletions in primate adult and embryonic stem cells. We propose the rhesus monkey to be an excellent model to assess the quality of gametes and embryos, as well as stem cells, and their developmental competence in human and non-human primates. This study was supported by National Institutes of Health grants RR15395 and HD045966.


Planta ◽  
2012 ◽  
Vol 237 (2) ◽  
pp. 509-515 ◽  
Author(s):  
Janina Apitz ◽  
Andreas Weihe ◽  
Frank Pohlheim ◽  
Thomas Börner

2018 ◽  
Author(s):  
Reena Debray ◽  
Noah Snyder-Mackler ◽  
Jordan Kohn ◽  
Mark Wilson ◽  
Luis Barreiro ◽  
...  

AbstractIn many social mammals, social adversity predicts compromised health and reduced fitness. These effects are thought to be driven in part by chronic social stress, but their molecular underpinnings are not well understood. Recent work suggests that chronic stress can affect mitochondrial copy number, heteroplasmy rates, and function. Here, we tested the first two possibilities, for the first time in nonhuman primates. We manipulated dominance rank in captive female rhesus macaques (n=45), where low rank induces chronic social stress, and measured mitochondrial DNA copy number and heteroplasmy in five peripheral blood mononuclear cell types from each study subject. We found no effect of dominance rank on either mtDNA copy number or heteroplasmy rates. However, grooming rates, a measure of affiliative social behavior predicted by high social status, was positively associated with mtDNA copy number in B cells, cytotoxic T cells, and monocytes. Our results suggest that social interactions can influence mtDNA regulation in immune cells. Further, they indicate the importance of considering both affiliative and competitive interactions in investigating this relationship.


2020 ◽  
Author(s):  
Jesse Slone ◽  
Weiwei Zou ◽  
Shiyu Luo ◽  
Eric S Schmitt ◽  
Stella Maris Chen ◽  
...  

ABSTRACTWith very few exceptions, mitochondrial DNA (mtDNA) in humans is transmitted exclusively from mothers to their offspring, suggesting the presence of a strong evolutionary pressure favoring the exclusion of paternal mtDNA. We have recently shown strong evidence of paternal mtDNA transmission. In these rare situations, males exhibiting biparental mtDNA appear to be limited to transmitting just one of the mtDNA species to their offspring, while females possessing biparental mtDNA populations consistently transmit both populations to their offspring at a very similar heteroplasmy level. The precise biological and genetic factors underlying this unusual transmission event remain unclear. Here, we have examined heteroplasmy levels in various tissues among individuals with biparental inheritance. Our results indicate that individuals with biparental mtDNA have remarkable inter-tissue variability in heteroplasmy level. At the single-cell level, paternal mtDNA heteroplasmy in sperm varies dramatically, and many sperm possess only one of the two mtDNA populations originally in question. These results show a fundamental, parent-of-origin difference in how mtDNA molecules transmit and propagate. This helps explain how a single population of mtDNAs are transmitted from a father possessing two populations of mtDNA molecules, suggesting that some mtDNA populations may be favored over others when transmitted from the father.


2009 ◽  
Vol 282 (6) ◽  
pp. 587-593 ◽  
Author(s):  
Andreas Weihe ◽  
Janina Apitz ◽  
Frank Pohlheim ◽  
Annabel Salinas-Hartwig ◽  
Thomas Börner

Science ◽  
1991 ◽  
Vol 251 (5000) ◽  
pp. 1488-1490 ◽  
Author(s):  
W. Hoeh ◽  
K. Blakley ◽  
W. Brown

2019 ◽  
Vol 15 (1) ◽  
pp. 20180643 ◽  
Author(s):  
Reena Debray ◽  
Noah Snyder-Mackler ◽  
Jordan N. Kohn ◽  
Mark E. Wilson ◽  
Luis B. Barreiro ◽  
...  

In many social mammals, social adversity predicts compromised health and reduced fitness. These effects are thought to be driven in part by chronic social stress, but their molecular underpinnings are not well understood. Recent work suggests that chronic stress can affect mitochondrial copy number, heteroplasmy rates and function. Here, we tested the first two possibilities for the first time in non-human primates. We manipulated dominance rank in captive female rhesus macaques ( n = 45), where low rank induces chronic social stress, and measured mitochondrial DNA (mtDNA) copy number and heteroplasmy in five peripheral blood mononuclear cell types from each study subject. We found no effect of dominance rank on either mtDNA copy number or heteroplasmy rates. However, grooming rate, a measure of affiliative social behaviour predicted by high social status, was positively associated with mtDNA copy number in B cells, cytotoxic T cells and monocytes. Our results suggest that social interactions can influence mtDNA regulation in immune cells. Further, they indicate the importance of considering both affiliative and competitive interactions in investigating this relationship.


Genetics ◽  
2003 ◽  
Vol 164 (3) ◽  
pp. 963-975 ◽  
Author(s):  
Y Moriyama ◽  
S Kawano

Abstract Although mitochondria are inherited uniparentally in nearly all eukaryotes, the mechanism for this is unclear. When zygotes of the isogamous protist Physarum polycephalum were stained with DAPI, the fluorescence of mtDNA in half of the mitochondria decreased simultaneously to give small spots and then disappeared completely ∼1.5 hr after nuclear fusion, while the other mitochondrial nucleoids and all of the mitochondrial sheaths remained unchanged. PCR analysis of single zygote cells confirmed that the loss was limited to mtDNA from one parent. The vacant mitochondrial sheaths were gradually eliminated by 60 hr after mating. Using six mating types, the transmission patterns of mtDNA were examined in all possible crosses. In 39 of 60 crosses, strict uniparental inheritance was confirmed in accordance with a hierarchy of relative sexuality. In the other crosses, however, mtDNA from both parents was transmitted to plasmodia. The ratio of parental mtDNA was estimated to be from 1:1 to 1:10-4. Nevertheless, the matA hierarchy was followed. In these crosses, the mtDNA was incompletely digested, and mtDNA replicated during subsequent plasmodial development. We conclude that the rapid, selective digestion of mtDNA promotes the uniparental inheritance of mitochondria; when this fails, biparental inheritance occurs.


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