The FASTK family proteins are master regulators in mitochondrial RNA processing
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA658336 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR12483652.fastq.gz | Fastqsanger.gz | |||
| SRR12483653.fastq.gz | Fastqsanger.gz | |||
| SRR12483654.fastq.gz | Fastqsanger.gz | |||
| SRR12483655.fastq.gz | Fastqsanger.gz | |||
| SRR12483656.fastq.gz | Fastqsanger.gz |
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Project description:Investigation of roles of the FASTK protein family in non-canonical mitochondrial RNA processing
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Project description:The FASTK family proteins are emerging key post-transcriptional regulators in mitochondrial gene expression. In attempts to uncover their molecular functions, we carried out BioID experiments to identify proteins interacting with FASTKD4 and FASTKD5. Our data suggest that both proteins have similar protein interactome profiles, highlighting their roles in mitochondrial RNA processing.
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2021-04-14 | GSE161133 | GEO
Project description:Canonical RNA processing in mammalian mitochondria necessitates that tRNAs are recognised by nucleases to release flanking transcripts. However, not all mitochondrial transcripts are punctuated by tRNAs, and the mechanism and factors involved in their processing has remained unsolved. Here, we demonstrate that phosphatase activity of the carbon catabolite repressor 4 domain containing family member ANGEL2 is required for the hydrolysis of 3′ phosphates, resulting from non-canonical processing. Interaction studies in Drosophila further identify that members of the FAST kinase domain containing protein family are involved in the formation of these 3′ phosphates. Our results therefore resolve the mechanism of RNA processing in metazoan mitochondria, by defining the outstanding non-canonical processing mechanism.
2022-09-04 | GSE189750 | GEO
Project description:Sphingolipids comprise a diverse family of lipids that perform multiple functions in both structure of cellular membranes and intra- and inter-cellular signaling. The diversity of this family is generated by an array of enzymes that produce individual classes and molecular species of family members and enzymes which catabolize those lipids for recycling pathways. However, all of these lipids begin their lives with a single step, the condensation of an amino acid, almost always serine, and a fatty acyl-CoA, almost always the 16-carbon, saturated fatty acid, palmitate. The enzyme complex that accomplishes this condensation is serine palmitoyltransferase (SPT), a membrane-bound component of the endoplasmic reticulum. This places SPT in the unique position of regulating the production of the entire sphingolipid pool. Understanding how SPT activity is regulated is currently a central focus in the field of sphingolipid biology. In this review we examine the regulation of SPT activity by a set of small, membrane-bound proteins of the endoplasmic reticulum, the Orms (in yeast) and ORMDLs (in vertebrates). We discuss what is known about how these proteins act as homeostatic regulators by monitoring cellular levels of sphingolipid, but also how the Orms/ORMDLs regulate SPT in response to other stimuli. Finally, we discuss the intriguing connection between one of the mammalian ORMDL isoforms, ORMDL3, and the pervasive pulmonary disease, asthma, in humans.
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Project description:Hierarchal gene master regulators of adenocarcinomic human alveolar basal epithelial cells A549.
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Project 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. Author summary As a legacy of their bacterial origin, mitochondria have retained their own genome with a unique gene expression system. All mitochondrially encoded proteins are essential components of the respiratory chain. Therefore, the mitochondrial gene expression is crucial for their iconic role as the ‘powerhouse of the cell’–ATP synthesis through oxidative phosphorylation. Consistently, defects in enzymes involved in this gene expression system are a common source of incurable inherited metabolic disorders, called mitochondrial diseases. The human mitochondrial transcription generates long polycistronic transcripts that carry information for multiple genes, so that the expression level of each gene is mainly regulated through post-transcriptional events. The polycistronic transcript first undergoes RNA processing, where individual mRNA, rRNA, and tRNA are cleaved off. However, its entire molecular mechanism remains unclear, and in particular, ‘non-canonical’ RNA processing has been poorly understood. To address this question, we studied the FASTK family proteins, emerging key mitochondrial post-transcriptional regulators. We generated different human cell lines carrying single or combined disruption of FASTKD3, FASTKD4, and FASTKD5 genes, and analyzed them using biochemical and genetic approaches. We show that the FASTK family members fine-tune the processing of both ‘canonical’ and ‘non-canonical’ mitochondrial RNA junctions.
| S-EPMC8601606 | biostudies-literature
Project description:The FASTK family proteins have recently emerged as key post-transcriptional regulators of mitochondrial gene expression. FASTK, the founding member and its homologs FASTKD1-5 are architecturally related RNA-binding proteins, each having a different function in the regulation of mitochondrial RNA biology, from mRNA processing and maturation to ribosome assembly and translation. In this review, we outline the structure, evolution and function of these FASTK proteins and discuss the individual role that each has in mitochondrial RNA biology. In addition, we highlight the aspects of FASTK research that still require more attention.
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