The FASTK family proteins fine-tune mitochondrial RNA processing.

Transcription of the human mitochondrial genome and correct processing of the two long polycistronic transcripts are crucial for oxidative phosphorylation. According to the tRNA punctuation model, nucleolytic processing of these large precursor transcripts occurs mainly through the excision of the t...

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Autores principales:	Akira Ohkubo, Lindsey Van Haute, Danielle L Rudler, Maike Stentenbach, Florian A Steiner, Oliver Rackham, Michal Minczuk, Aleksandra Filipovska, Jean-Claude Martinou
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2021
Materias:	Genetics QH426-470
Acceso en línea:	https://doaj.org/article/4c5c70293ada4f08931022703464602a
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spelling	oai:doaj.org-article:4c5c70293ada4f08931022703464602a2021-12-02T20:03:15ZThe FASTK family proteins fine-tune mitochondrial RNA processing.1553-73901553-740410.1371/journal.pgen.1009873https://doaj.org/article/4c5c70293ada4f08931022703464602a2021-11-01T00:00:00Zhttps://doi.org/10.1371/journal.pgen.1009873https://doaj.org/toc/1553-7390https://doaj.org/toc/1553-7404Transcription of the human mitochondrial genome and correct processing of the two long polycistronic transcripts are crucial for oxidative phosphorylation. According to the tRNA punctuation model, nucleolytic processing of these large precursor transcripts occurs mainly through the excision of the tRNAs that flank most rRNAs and mRNAs. However, some mRNAs are not punctuated by tRNAs, and it remains largely unknown how these non-canonical junctions are resolved. The FASTK family proteins are emerging as key players in non-canonical RNA processing. Here, we have generated human cell lines carrying single or combined knockouts of several FASTK family members to investigate their roles in non-canonical RNA processing. The most striking phenotypes were obtained with loss of FASTKD4 and FASTKD5 and with their combined double knockout. Comprehensive mitochondrial transcriptome analyses of these cell lines revealed a defect in processing at several canonical and non-canonical RNA junctions, accompanied by an increase in specific antisense transcripts. Loss of FASTKD5 led to the most severe phenotype with marked defects in mitochondrial translation of key components of the electron transport chain complexes and in oxidative phosphorylation. We reveal that the FASTK protein family members are crucial regulators of non-canonical junction and non-coding mitochondrial RNA processing.Akira OhkuboLindsey Van HauteDanielle L RudlerMaike StentenbachFlorian A SteinerOliver RackhamMichal MinczukAleksandra FilipovskaJean-Claude MartinouPublic Library of Science (PLoS)articleGeneticsQH426-470ENPLoS Genetics, Vol 17, Iss 11, p e1009873 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Genetics QH426-470
spellingShingle	Genetics QH426-470 Akira Ohkubo Lindsey Van Haute Danielle L Rudler Maike Stentenbach Florian A Steiner Oliver Rackham Michal Minczuk Aleksandra Filipovska Jean-Claude Martinou The FASTK family proteins fine-tune mitochondrial RNA processing.
description	Transcription of the human mitochondrial genome and correct processing of the two long polycistronic transcripts are crucial for oxidative phosphorylation. According to the tRNA punctuation model, nucleolytic processing of these large precursor transcripts occurs mainly through the excision of the tRNAs that flank most rRNAs and mRNAs. However, some mRNAs are not punctuated by tRNAs, and it remains largely unknown how these non-canonical junctions are resolved. The FASTK family proteins are emerging as key players in non-canonical RNA processing. Here, we have generated human cell lines carrying single or combined knockouts of several FASTK family members to investigate their roles in non-canonical RNA processing. The most striking phenotypes were obtained with loss of FASTKD4 and FASTKD5 and with their combined double knockout. Comprehensive mitochondrial transcriptome analyses of these cell lines revealed a defect in processing at several canonical and non-canonical RNA junctions, accompanied by an increase in specific antisense transcripts. Loss of FASTKD5 led to the most severe phenotype with marked defects in mitochondrial translation of key components of the electron transport chain complexes and in oxidative phosphorylation. We reveal that the FASTK protein family members are crucial regulators of non-canonical junction and non-coding mitochondrial RNA processing.
format	article
author	Akira Ohkubo Lindsey Van Haute Danielle L Rudler Maike Stentenbach Florian A Steiner Oliver Rackham Michal Minczuk Aleksandra Filipovska Jean-Claude Martinou
author_facet	Akira Ohkubo Lindsey Van Haute Danielle L Rudler Maike Stentenbach Florian A Steiner Oliver Rackham Michal Minczuk Aleksandra Filipovska Jean-Claude Martinou
author_sort	Akira Ohkubo
title	The FASTK family proteins fine-tune mitochondrial RNA processing.
title_short	The FASTK family proteins fine-tune mitochondrial RNA processing.
title_full	The FASTK family proteins fine-tune mitochondrial RNA processing.
title_fullStr	The FASTK family proteins fine-tune mitochondrial RNA processing.
title_full_unstemmed	The FASTK family proteins fine-tune mitochondrial RNA processing.
title_sort	fastk family proteins fine-tune mitochondrial rna processing.
publisher	Public Library of Science (PLoS)
publishDate	2021
url	https://doaj.org/article/4c5c70293ada4f08931022703464602a
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The FASTK family proteins fine-tune mitochondrial RNA processing.

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