Abstract：
:Mutations of mtDNA cause mitochondrial diseases and are implicated in age-associated diseases and aging. Pathogenic mtDNA mutations are often present in a fraction of all mtDNA copies, and it has been widely debated whether the proportion of mutant genomes or the absolute number of wild-type molecules determines if oxidative phosphorylation (OXPHOS) will be impaired. Here, we have studied the male infertility phenotype of mtDNA mutator mice and demonstrate that decreasing mtDNA copy number worsens mitochondrial aberrations of spermatocytes and spermatids in testes, whereas an increase in mtDNA copy number rescues the fertility phenotype and normalizes testes morphology as well as spermatocyte proteome changes. The restoration of testes function occurs in spite of unaltered total mtDNA mutation load. We thus demonstrate that increased copy number of mtDNA can efficiently ameliorate a severe disease phenotype caused by mtDNA mutations, which has important implications for developing future strategies for treatment of mitochondrial dysfunction.
journal_name
Cell Metabjournal_title
Cell metabolismauthors
Jiang M,Kauppila TES,Motori E,Li X,Atanassov I,Folz-Donahue K,Bonekamp NA,Albarran-Gutierrez S,Stewart JB,Larsson NGdoi
10.1016/j.cmet.2017.07.003subject
Has Abstractpub_date
2017-08-01 00:00:00pages
429-436.e4issue
2eissn
1550-4131issn
1932-7420pii
S1550-4131(17)30424-2journal_volume
26pub_type
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