scholarly journals Human mitochondrial DNA with large deletions repopulates organelles faster than full-length genomes under relaxed copy number control

2002 ◽  
Vol 30 (21) ◽  
pp. 4626-4633 ◽  
Author(s):  
F. Diaz
2000 ◽  
Vol 11 (4) ◽  
pp. 1471-1485 ◽  
Author(s):  
Yingying Tang ◽  
Eric A. Schon ◽  
Ekkehard Wilichowski ◽  
Martel E. Vazquez-Memije ◽  
Edgar Davidson ◽  
...  

Mitochondria from patients with Kearns–Sayre syndrome harboring large-scale rearrangements of human mitochondrial DNA (mtDNA; both partial deletions and a partial duplication) were introduced into human cells lacking endogenous mtDNA. Cytoplasmic hybrids containing 100% wild-type mtDNA, 100% mtDNA with partial duplications, and 100% mtDNA with partial deletions were isolated and characterized. The cell lines with 100% deleted mtDNAs exhibited a complete impairment of respiratory chain function and oxidative phosphorylation. In contrast, there were no detectable respiratory chain or protein synthesis defects in the cell lines with 100% duplicated mtDNAs. Unexpectedly, the mass of mtDNA was identical in all cell lines, despite the fact that different lines contained mtDNAs of vastly different sizes and with different numbers of replication origins, suggesting that mtDNA copy number may be regulated by tightly controlled mitochondrial dNTP pools. In addition, quantitation of mtDNA-encoded RNAs and polypeptides in these lines provided evidence that mtDNA gene copy number affects gene expression, which, in turn, is regulated at both the post-transcriptional and translational levels.


Mitochondrion ◽  
2018 ◽  
Vol 38 ◽  
pp. 41-47 ◽  
Author(s):  
Shan Gao ◽  
Xiaoxuan Tian ◽  
Hong Chang ◽  
Yu Sun ◽  
Zhenfeng Wu ◽  
...  

2019 ◽  
Author(s):  
Wioletta Czaja ◽  
Douda Bensasson ◽  
Hyo Won Ahn ◽  
David J. Garfinkel ◽  
Casey M. Bergman

AbstractInsertion of mobile DNA sequences typically has deleterious effects on host fitness, and thus diverse mechanisms have evolved to control mobile element proliferation across the tree of life. Mobility of the Ty1 retrotransposon in Saccharomyces yeasts is regulated by a novel form of copy number control (CNC) mediated by a self-encoded restriction factor derived from the Ty1 gag capsid gene that inhibits virus-like particle function. Here, we survey a panel of wild and human-associated strains of S. cerevisiae and S. paradoxus to investigate how genomic Ty1 content influences variation in Ty1 mobility. We observe high levels of mobility for a canonical Ty1 tester element in permissive strains that either lack full-length Ty1 elements or only contain full-length copies of the Ty1’ subfamily that have a divergent gag sequence. In contrast, low levels of canonical Ty1 mobility are observed in restrictive strains carrying full-length Ty1 elements containing canonical gag. Phylogenomic analysis of full-length Ty1 elements revealed that Ty1’ is the ancestral subfamily present in wild strains of S. cerevisiae, and that canonical Ty1 in S. cerevisiae is a derived subfamily that acquired gag from S. paradoxus by horizontal transfer and recombination. Our results provide evidence that variation in the ability of S. cerevisiae and S. paradoxus strains to repress canonical Ty1 transposition via CNC is encoded by the genomic content of different Ty1 subfamilies, and that self-encoded forms of transposon control can spread across species boundaries by horizontal transfer.


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