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学術論文

Mammalian transcription factor A is a core component of the mitochondrial transcription machinery.

MPS-Authors

Shi,  Yonghong
Max Planck Society;

Dierckx,  Anke
Max Planck Society;

Wanrooij,  Paulina H
Max Planck Society;

Wanrooij,  Sjoerd
Max Planck Society;

Larsson,  Nils-Göran
Max Planck Society;

Wilhelmsson,  L Marcus
Max Planck Society;

Falkenberg,  Maria
Max Planck Society;

Gustafsson,  Claes M
Max Planck Society;

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引用

Shi, Y., Dierckx, A., Wanrooij, P. H., Wanrooij, S., Larsson, N.-G., Wilhelmsson, L. M., Falkenberg, M., & Gustafsson, C. M. (2012). Mammalian transcription factor A is a core component of the mitochondrial transcription machinery. Proc Natl Acad Sci USA, 109(41), 16510-16515.


引用: http://hdl.handle.net/11858/00-001M-0000-0028-59B0-8
要旨
Transcription factor A (TFAM) functions as a DNA packaging factor in mammalian mitochondria. TFAM also binds sequence-specifically to sites immediately upstream of mitochondrial promoters, but there are conflicting data regarding its role as a core component of the mitochondrial transcription machinery. We here demonstrate that TFAM is required for transcription in mitochondrial extracts as well as in a reconstituted in vitro transcription system. The absolute requirement of TFAM can be relaxed by conditions that allow DNA breathing, i.e., low salt concentrations or negatively supercoiled DNA templates. The situation is thus very similar to that described in nuclear RNA polymerase II-dependent transcription, in which the free energy of supercoiling can circumvent the need for a subset of basal transcription factors at specific promoters. In agreement with these observations, we demonstrate that TFAM has the capacity to induce negative supercoils in DNA, and, using the recently developed nucleobase analog FRET-pair tC(O)-tC(nitro), we find that TFAM distorts significantly the DNA structure. Our findings differ from recent observations reporting that TFAM is not a core component of the mitochondrial transcription machinery. Instead, our findings support a model in which TFAM is absolutely required to recruit the transcription machinery during initiation of transcription.