ArticleNucleic acids research2011
PDE12 removes mitochondrial RNA poly(A) tails and controls translation in human mitochondria.
Article in Nucleic acids research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.
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65 citing papers in PubMed, 104 citations in OpenAlex.
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- ANGEL2 phosphatase activity is required for non-canonical mitochondrial RNA processing.Nature communications · 2022Article
- How RNases Shape Mitochondrial Transcriptomes.International journal of molecular sciences · 2022Review
- Non-coding RNAs: The Neuroinflammatory Regulators in Neurodegenerative Diseases.Frontiers in neurology · 2022Review
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- Purification of Mitochondrial Ribosomes with the Translocase Oxa1L from HEK Cells.Bio-protocol · 2021Article
- YbeY is required for ribosome small subunit assembly and tRNA processing in human mitochondria.Nucleic acids research · 2021Article
- Mechanisms and regulation of protein synthesis in mitochondria.Nature reviews. Molecular cell biology · 2021Review
- Functions and mechanisms of RNA tailing by metazoan terminal nucleotidyltransferases.Wiley interdisciplinary reviews. RNA · 2021Review
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- Co-expression analysis identifies neuro-inflammation as a driver of sensory neuron aging in Aplysia californica.PloS one · 2021Article
- Differential processing and localization of human Nocturnin controls metabolism of mRNA and nicotinamide adenine dinucleotide cofactors.The Journal of biological chemistry · 2020Article
- New advances in our understanding of the "unique" RNase L in host pathogen interaction and immune signaling.Cytokine · 2020Review
- Mechanism of ribosome rescue by alternative ribosome-rescue factor B.Nature communications · 2020Article
5 more citing papers are in PubMed but not listed here.
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3 authors at 2 institutions in 1 country.
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Abstract
Polyadenylation of mRNA in human mitochondria is crucial for gene expression and perturbation of poly(A) tail length has been linked to a human neurodegenerative disease. Here we show that 2'-phosphodiesterase (2'-PDE), (hereafter PDE12), is a mitochondrial protein that specifically removes poly(A) extensions from mitochondrial mRNAs both in vitro and in mitochondria of cultured cells. In eukaryotes, poly(A) tails generally stabilize mature mRNAs, whereas in bacteria they increase mRNA turnover. In human mitochondria, the effects of increased PDE12 expression were transcript dependent. An excess of PDE12 led to an increase in the level of three mt-mRNAs (ND1, ND2 and CytB) and two (CO1 and CO2) were less abundant than in mitochondria of control cells and there was no appreciable effect on the steady-state level of the remainder of the mitochondrial transcripts. The alterations in poly(A) tail length accompanying elevated PDE12 expression were associated with severe inhibition of mitochondrial protein synthesis, and consequently respiratory incompetence. Therefore, we propose that mRNA poly(A) tails are important in regulating protein synthesis in human mitochondria, as it is the case for nuclear-encoded eukaryotic mRNA.
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