2004
DOI: 10.1074/jbc.m401643200
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Drosophila Mitochondrial Transcription Factor B2 Regulates Mitochondrial DNA Copy Number and Transcription in Schneider Cells

Abstract: We report the cloning and molecular analysis of Drosophila mitochondrial transcription factor B2 (d-mt-TFB2), a protein that plays a role in mitochondrial transcription and mitochondrial DNA (mtDNA) replication in Drosophila. An RNA interference (RNAi) construct was designed that reduces expression of d-mtTFB2 to 5% of its normal level in Schneider cells. RNAi knock-down of d-mtTFB2 reduces the abundance of specific mitochondrial RNA transcripts 2-to 8-fold and decreases the copy number of mtDNA ϳ3-fold. In a … Show more

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Cited by 77 publications
(79 citation statements)
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“…These results indicate that mtDNA is in excess of that needed for normal mitochondrial transcription in Schneider cells. Similar results were obtained upon either suppression or overexpression of the mitochondrial transcription factor A (25,30,31). These data contrast with our finding that mitochondrial transcription factor B2 regulates directly both mtDNA copy number and transcription (25), whereas mitochondrial transcription factor B1 affects neither mtDNA nor transcript levels (26).…”
Section: Discussioncontrasting
confidence: 57%
“…These results indicate that mtDNA is in excess of that needed for normal mitochondrial transcription in Schneider cells. Similar results were obtained upon either suppression or overexpression of the mitochondrial transcription factor A (25,30,31). These data contrast with our finding that mitochondrial transcription factor B2 regulates directly both mtDNA copy number and transcription (25), whereas mitochondrial transcription factor B1 affects neither mtDNA nor transcript levels (26).…”
Section: Discussioncontrasting
confidence: 57%
“…The TFB1M isoform is transiently down-regulated relative to that of the TFB2M isoform in serum-stimulated quiescent fibroblasts, suggesting that the latter is favored in the transition to proliferative growth (19). RNA-mediated interference knockdown of the Drosophila B2 isoform results in reduced mtDNA transcription and copy number (43). This contrasts with RNA-mediated interference knockdown of the B1 isoform, which has no effect on mtDNA transcription or replication but does result in reduced mitochondrial translation (44).…”
Section: Discussioncontrasting
confidence: 44%
“…However, unlike T7 RNA polymerase, which does not require any transcription factors, efficient promoter-specific initiation by human POLRMT in vitro requires the high mobility group box transcription factor h-mtTFA/TFAM (referred to as h-mtTFA from this point forward) and one of two rRNA methyltransferase-related transcription factors, h-mtTFB1 and h-mtTFB2 (11)(12)(13)(14). Based on work in Drosophila (15,16), cultured human cells (17,18), and mice (19), it is becoming clear that, whereas both h-mtTFB1 and h-mtTFB2 can bind POLRMT and activate transcription in vitro, h-mtTFB2 is probably the primary transcription factor in vivo, whereas h-mtTFB1 is the primary rRNA methyltransferase critical for mitochondrial ribosome biogenesis and translation. However, both proteins have retained both activities (20,21) and act in concert to promote normal mitochondrial biogenesis, gene expression, and activity (17).…”
mentioning
confidence: 99%