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Lu, Bin; Lee, Jae; Nie, Xiaobo; Li, Min; Morozov, Yaroslav I.; Venkatesh, Sundararajan; Bogenhagen, Daniel F.; Temiakov, Dmitry; Suzuki, Carolyn K.
Molecular cell, 01/2013, Letnik: 49, Številka: 1Journal Article
Human mitochondrial transcription factor A (TFAM) is a high-mobility group (HMG) protein at the nexus of mitochondrial DNA (mtDNA) replication, transcription, and inheritance. Little is known about the mechanisms underlying its posttranslational regulation. Here, we demonstrate that TFAM is phosphorylated within its HMG box 1 (HMG1) by cAMP-dependent protein kinase in mitochondria. HMG1 phosphorylation impairs the ability of TFAM to bind DNA and to activate transcription. We show that only DNA-free TFAM is degraded by the Lon protease, which is inhibited by the anticancer drug bortezomib. In cells with normal mtDNA levels, HMG1-phosphorylated TFAM is degraded by Lon. However, in cells with severe mtDNA deficits, nonphosphorylated TFAM is also degraded, as it is DNA free. Depleting Lon in these cells increases levels of TFAM and upregulates mtDNA content, albeit transiently. Phosphorylation and proteolysis thus provide mechanisms for rapid fine-tuning of TFAM function and abundance in mitochondria, which are crucial for maintaining and expressing mtDNA. Display omitted ► cAMP-dependent protein kinase (PKA) serine phosphorylates TFAM within HMG1 ► HMG1 phosphorylation of TFAM impairs DNA binding and transcription activation ► Lon protease selectively degrades DNA-free TFAM and is inhibited by bortezomib ► Lon knockdown stabilizes TFAM in mtDNA-deficient cells and upregulates mtDNA
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