期刊
NUCLEIC ACIDS RESEARCH
卷 37, 期 17, 页码 5701-5713出版社
OXFORD UNIV PRESS
DOI: 10.1093/nar/gkp614
关键词
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资金
- UK Medical Research Council
- Academy of Finland [110689, 103213, 110463, 108380]
- CoE funding
- Juselius Foundation
- Tampere University Hospital Medical Research Fund
- University of Tampere
- European Union FP6
- Mitocombat Integrated Programme
- UK Muscular Dystrophy Campaign
- Medical Research Council
- Academy of Finland (AKA) [103213, 108380, 110689, 110463, 108380, 110463, 110689, 103213] Funding Source: Academy of Finland (AKA)
- Medical Research Council [MC_U105663140, MC_U105474168] Funding Source: researchfish
- MRC [MC_U105663140, MC_U105474168] Funding Source: UKRI
The accessory subunit of mitochondrial DNA polymerase gamma, POLG beta, functions as a processivity factor in vitro. Here we show POLG beta has additional roles in mitochondrial DNA metabolism. Mitochondrial DNA is arranged in nucleoprotein complexes, or nucleoids, which often contain multiple copies of the mitochondrial genome. Gene-silencing of POLG beta increased nucleoid numbers, whereas overexpression of POLG beta reduced the number and increased the size of mitochondrial nucleoids. Both increased and decreased expression of POLG beta altered nucleoid structure and precipitated a marked decrease in 7S DNA molecules, which form short displacement-loops on mitochondrial DNA. Recombinant POLG beta preferentially bound to plasmids with a short displacement-loop, in contrast to POLG alpha. These findings support the view that the mitochondrial D-loop acts as a protein recruitment centre, and suggest POLG beta is a key factor in the organization of mitochondrial DNA in multigenomic nucleoprotein complexes.
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