ArticleMolecular genetics and metabolism reports2020
Poly (A) tail length of human mitochondrial mRNAs is tissue-specific and a mutation in LRPPRC results in transcript-specific patterns of deadenylation.
Article in Molecular genetics and metabolism reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 19 citations in OpenAlex.
- Folding the message: mRNA structure as a regulatory layer of human mitochondrial gene expression.Biochimica et biophysica acta. Molecular cell research · 2026Review
- ReducedbioRxiv : the preprint server for biology · 2026Article
- Molecular glue that stabilizes the LRPPRC-MET-G4 interaction complex to drive MET downregulation.Nature communications · 2026Article
- Largely Distinct Post-Translational Modifications Differentiate Skeletal Muscle Wasting Caused by Cancer, Dexamethasone and Aging.Journal of cachexia, sarcopenia and muscle · 2026Article
- Article
- The human mitochondrial mRNA structurome reveals mechanisms of gene expression.Science (New York, N.Y.) · 2024Article
- Review
- Mitochondrial protein synthesis quality control.Human molecular genetics · 2024Review
- RNA binding proteins in cardiovascular development and disease.Current topics in developmental biology · 2024Article
- Mitochondrial nucleic acids in innate immunity and beyond.Experimental & molecular medicine · 2023Review
- RNA binding protein: coordinated expression between the nuclear and mitochondrial genomes in tumors.Journal of translational medicine · 2023Review
- The RNA-binding protein LRPPRC promotes resistance to CDK4/6 inhibition in lung cancer.Nature communications · 2023Article
- A small protein coded within the mitochondrial canonical gene nd4 regulates mitochondrial bioenergetics.BMC biology · 2023Article
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mutations in LRPPRC cause Leigh Syndrome French Canadian (LSFC), an early onset neurodegenerative disease, with differential tissue involvement. The molecular basis for tissue specificity in this disease remains unknown. LRPPRC, an RNA binding protein, forms a stable complex with SLIRP, which binds to, and stabilizes mitochondrial mRNAs. In cell culture and animal models, loss of LRPPRC function results in transcript-specific alterations in the steady-state levels of mitochondrial mRNAs and poly (A) tail length, the mechanisms for which are not understood. The poly (A) tail length of mitochondrial mRNAs has not been investigated in human tissues from heathy subjects or LSFC patients. Here we have mapped the 3'-termini of mature mitochondrial mRNAs in three tissues (skeletal muscle, heart, and liver) from a healthy individual and an LSFC patient. We show that the poly (A) tail length of mitochondrial mRNAs varies amongst tissues, and that the missense mutation in LRPPRC that causes LSFC results in tissue- and transcript-specific deadenylation of a subset of mitochondrial mRNAs, likely contributing the nature and severity of the biochemical phenotype in different tissues. We also found a relatively large fraction of short transcripts lacking a stop codon, some with short poly (A) tails, in patient tissue, suggesting that mutations in LRPPRC may also impair proper 3' end processing of some mRNAs.
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