ArticleThe Journal of biological chemistry2013
The leucine-rich pentatricopeptide repeat-containing protein (LRPPRC) does not activate transcription in mammalian mitochondria.
Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 34 citations in OpenAlex.
- POLRMT overexpression increases mtDNA transcription without affecting steady-state mRNA levels.Life science alliance · 2025Article
- LRPPRC and SLIRP synergize to maintain sufficient and orderly mammalian mitochondrial translation.Nucleic acids research · 2024Article
- Illuminating mitochondrial translation through mouse models.Human molecular genetics · 2024Review
- Pathological and Therapeutic Advances in Parkinson's Disease: Mitochondria in the Interplay.Journal of Alzheimer's disease : JAD · 2023Review
- LRPPRC-mediated folding of the mitochondrial transcriptome.Nature communications · 2017Article
- Drosophila protease ClpXP specifically degrades DmLRPPRC1 controlling mitochondrial mRNA and translation.Scientific reports · 2017Article
- SLIRP stabilizes LRPPRC via an RRM-PPR protein interface.Nucleic acids research · 2016Article
- POLRMT regulates the switch between replication primer formation and gene expression of mammalian mtDNA.Science advances · 2016Article
- Increased Hepatic Fatty Acids Uptake and Oxidation by LRPPRC-Driven Oxidative Phosphorylation Reduces Blood Lipid Levels.Frontiers in physiology · 2016Article
- Overexpression of the mitochondrial methyltransferase TFB1M in the mouse does not impact mitoribosomal methylation status or hearing.Human molecular genetics · 2015Article
- SLIRP Regulates the Rate of Mitochondrial Protein Synthesis and Protects LRPPRC from Degradation.PLoS genetics · 2015Article
- Mitochondrial transcript maturation and its disorders.Journal of inherited metabolic disease · 2015Review
- Mitochondrial Diseases Part II: Mouse models of OXPHOS deficiencies caused by defects in regulatory factors and other components required for mitochondrial function.Mitochondrion · 2015Review
- Drosophila melanogaster LRPPRC2 is involved in coordination of mitochondrial translation.Nucleic acids research · 2014Article
- Energizing Genetics and Epi-genetics: Role in the Regulation of Mitochondrial Function.Current genomics · 2014Article
- Functional genomic analysis of human mitochondrial RNA processing.Cell reports · 2014Article
- Mitochondria: impaired mitochondrial translation in human disease.The international journal of biochemistry & cell biology · 2014Review
- The Biological Role of LRPPRC in Human Cancers.Cancer control : journal of the Moffitt Cancer CenterReview
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Regulation of mtDNA expression is critical for controlling oxidative phosphorylation capacity and has been reported to occur at several different levels in mammalian mitochondria. LRPPRC (leucine-rich pentatricopeptide repeat-containing protein) has a key role in this regulation and acts at the post-transcriptional level to stabilize mitochondrial mRNAs, to promote mitochondrial mRNA polyadenylation, and to coordinate mitochondrial translation. However, recent studies have suggested that LRPPRC may have an additional intramitochondrial role by directly interacting with the mitochondrial RNA polymerase POLRMT to stimulate mtDNA transcription. In this study, we have further examined the intramitochondrial roles for LRPPRC by creating bacterial artificial chromosome transgenic mice with moderately increased LRPPRC expression and heterozygous Lrpprc knock-out mice with moderately decreased LRPPRC expression. Variation of LRPPRC levels in mice in vivo, occurring within a predicted normal physiological range, strongly affected the levels of an unprocessed mitochondrial precursor transcript (ND5-cytochrome b) but had no effect on steady-state levels of mitochondrial transcripts or de novo transcription of mtDNA. We further assessed the role of LRPPRC in mitochondrial transcription by performing size exclusion chromatography and immunoprecipitation experiments in human cell lines and mice, but we found no interaction between LRPPRC and POLRMT. Furthermore, addition of purified LRPPRC to a recombinant human in vitro transcription system did not activate mtDNA transcription. On the basis of these data, we conclude that LRPPRC does not directly regulate mtDNA transcription but rather acts as a post-transcriptional regulator of mammalian mtDNA expression.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.