期刊
MOLECULAR CELL
卷 76, 期 5, 页码 784-+出版社
CELL PRESS
DOI: 10.1016/j.molcel.2019.09.010
关键词
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资金
- Swedish Research Council [2015-00418, 2018-02439, 2018-02579, 2017-01257]
- Swedish Cancer Foundation [2016-816, 2016-599, 2017-631, 2018-602]
- Knut and Alice Wallenberg Foundation [KAW 2017.0080, KAW 2016.0050]
- European Research Council [683191, 741366]
- Swedish government
- ALF [ALFGBG-727491, ALFGBG-728151, SLL2018.0471]
- National Health and Medical Research Council
- Australian Research Council
- Cancer Council of WA
- Wellcome Trust [213464/Z/18/Z]
- Royal Society [213464/Z/18/Z]
- Rosetrees and Stoneygate Trust Research Fellowship [M811]
- Wellcome Trust [213464/Z/18/Z] Funding Source: Wellcome Trust
- Swedish Research Council [2018-02439, 2018-02579, 2017-01257] Funding Source: Swedish Research Council
- European Research Council (ERC) [683191, 741366] Funding Source: European Research Council (ERC)
- Formas [2018-02439] Funding Source: Formas
Oligoribonucleases are conserved enzymes that degrade short RNA molecules of up to 5 nt in length and are assumed to constitute the final stage of RNA turnover. Here we demonstrate that REXO2 is a specialized dinucleotide-degrading enzyme that shows no preference between RNA and DNA dinucleotide substrates. A heart- and skeletal-muscle-specific knockout mouse displays elevated dinucleotide levels and alterations in gene expression patterns indicative of aberrant dinucleotide-primed transcription initiation. We find that dinucleotides act as potent stimulators of mitochondrial transcription initiation in vitro. Our data demonstrate that increased levels of dinucleotides can be used to initiate transcription, leading to an increase in transcription levels from both mitochondrial promoters and other, nonspecific sequence elements in mitochondrial DNA. Efficient RNA turnover by REXO2 is thus required to maintain promoter specificity and proper regulation of transcription in mammalian mitochondria.
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