Random genetic drift in the female germline explains the rapid segregation of mammalian mitochondrial DNA

1996 ◽  
Vol 14 (2) ◽  
pp. 146-151 ◽  
Author(s):  
Jack P. Jenuth ◽  
Alan C. Peterson ◽  
Katherine Fu ◽  
Eric A. Shoubridge
Life ◽  
2021 ◽  
Vol 11 (2) ◽  
pp. 76
Author(s):  
Elvira G. Zakirova ◽  
Vladimir V. Muzyka ◽  
Ilya O. Mazunin ◽  
Konstantin E. Orishchenko

The generally accepted theory of the genetic drift of mitochondrial alleles during mammalian ontogenesis is based on the presence of a selective bottleneck in the female germline. However, there is a variety of different theories on the pathways of genetic regulation of mitochondrial DNA (mtDNA) dynamics in oogenesis and adult somatic cells. The current review summarizes present knowledge on the natural mechanisms of mitochondrial genome elimination during mammalian development. We also discuss the variety of existing and developing methodologies for artificial manipulation of the mtDNA heteroplasmy level. Understanding of the basics of mtDNA dynamics will shed the light on the pathogenesis and potential therapies of human diseases associated with mitochondrial dysfunction.


Genetics ◽  
1992 ◽  
Vol 132 (1) ◽  
pp. 205-209 ◽  
Author(s):  
S Kambhampati ◽  
K S Rai ◽  
D M Verleye

Abstract A laboratory cage experiment was undertaken to study changes over time in the frequencies of two mitochondrial DNA (mtDNA) haplotypes in the mosquito, Aedes albopictus, under two conditions: bidirectionally compatible matings and unidirectionally incompatible matings. Frequencies were monitored for 10 generations in three replicate cages for each of the two conditions above. In cages with bidirectionally compatible strains, changes in haplotype frequencies were nondirectional and neither haplotype increased in frequency. Statistical analysis of relative proportions of the two haplotypes in each generation indicated that the magnitude of the observed fluctuations could be expected under an assumption of random genetic drift alone. In cages with unidirectionally incompatible matings, mtDNA of females that lay inviable eggs upon mating with males of another strain, decreased significantly in the F1 generation and was completely replaced in the F2 generation.


2017 ◽  
Author(s):  
Alexander Hübner ◽  
Manja Wachsmuth ◽  
Roland Schröder ◽  
Mingkun Li ◽  
Anna Maria Eis-Hübinger ◽  
...  

ABSTRACTMitochondrial DNA (mtDNA) heteroplasmy (intra-individual variation) varies among different human tissues and increases with age, suggesting that the majority of mtDNA heteroplasmies are acquired, rather than inherited. However, the extent to which heteroplasmic sites are shared across a tissue remains an open question. We therefore investigated heteroplasmy in two liver samples (one from each primary lobe) from 83 Europeans, sampled at autopsy. Minor allele frequencies (MAF) at heteroplasmic sites were significantly correlated between the two liver samples from an individual, with significantly more sharing of heteroplasmic sites in the control region than in the coding region. We show that this increased sharing for the control region cannot be explained by recent mutations at just a few specific heteroplasmic sites or by the possible presence of 7S DNA. Moreover, we carried out simulations to show that there is significantly more sharing than would be predicted from random genetic drift from a common progenitor cell. We also observe a significant excess of non-synonymous vs. synonymous heteroplasmies in the coding region, but significantly more sharing of synonymous heteroplasmies. These contrasting patterns for the control vs. the coding region, and for non-synonymous vs. synonymous heteroplasmies, suggest that selection plays a role in heteroplasmy sharing.


2008 ◽  
Vol 83 (5) ◽  
pp. 582-593 ◽  
Author(s):  
Passorn Wonnapinij ◽  
Patrick F. Chinnery ◽  
David C. Samuels

Evolution ◽  
2006 ◽  
Vol 60 (4) ◽  
pp. 643 ◽  
Author(s):  
Michael J. Wade ◽  
Charles J. Goodnight

Genetics ◽  
2004 ◽  
Vol 166 (3) ◽  
pp. 1155-1164 ◽  
Author(s):  
Daniel Shriner ◽  
Raj Shankarappa ◽  
Mark A. Jensen ◽  
David C. Nickle ◽  
John E. Mittler ◽  
...  

2016 ◽  
Vol 27 (4) ◽  
pp. 467-492 ◽  
Author(s):  
Tat Dat Tran ◽  
Julian Hofrichter ◽  
Jürgen Jost

2018 ◽  
Author(s):  
Antonios Kioukis ◽  
Pavlos Pavlidis

The evolution of a population by means of genetic drift and natural selection operating on a gene regulatory network (GRN) of an individual has not been scrutinized in depth. Thus, the relative importance of various evolutionary forces and processes on shaping genetic variability in GRNs is understudied. Furthermore, it is not known if existing tools that identify recent and strong positive selection from genomic sequences, in simple models of evolution, can detect recent positive selection when it operates on GRNs. Here, we propose a simulation framework, called EvoNET, that simulates forward-in-time the evolution of GRNs in a population. Since the population size is finite, random genetic drift is explicitly applied. The fitness of a mutation is not constant, but we evaluate the fitness of each individual by measuring its genetic distance from an optimal genotype. Mutations and recombination may take place from generation to generation, modifying the genotypic composition of the population. Each individual goes through a maturation period, where its GRN reaches equilibrium. At the next step, individuals compete to produce the next generation. As time progresses, the beneficial genotypes push the population higher in the fitness landscape. We examine properties of the GRN evolution such as robustness against the deleterious effect of mutations and the role of genetic drift. We confirm classical results from Andreas Wagner’s work that GRNs show robustness against mutations and we provide new results regarding the interplay between random genetic drift and natural selection.


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