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The Translation Initiation Factor Homolog, eif4e1c, Regulates Cardiomyocyte Metabolism and Proliferation During Heart Regeneration.

ABSTRACT: The Translation Initiation Factor Homolog, eif4e1c, Regulates Cardiomyocyte Metabolism and Proliferation During Heart Regeneration.

PROVIDER: PRJNA872137 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21218371.fastq.gz	Fastqsanger.gz
	SRR21218372.fastq.gz	Fastqsanger.gz
	SRR21218373.fastq.gz	Fastqsanger.gz
	SRR21218374.fastq.gz	Fastqsanger.gz
	SRR21218375.fastq.gz	Fastqsanger.gz

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The Translation Initiation Factor Homolog, eif4e1c, Regulates Cardiomyocyte Metabolism and Proliferation During Heart Regeneration.

Project description:The eIF4E family of translation initiation factors bind 5’ methylated caps and act as the limiting-step for mRNA translation. The canonical eIF4E1A is required for cell viability, yet other related families exist and are all utilized in specific contexts or tissues. Here, we describe a new family called Eif4e1c that is ancestral to the canonical eIF4E1A in vertebrates, and for which we find roles during heart development and regeneration in zebrafish. The Eif4e1c family is present in all aquatic vertebrates but has been lost in all terrestrial species. A core group of amino acids shared over 500 million years of evolution from ray-finned fish to sharks forms an evolutionarily conserved binding interface along the surface of the protein, suggesting Eif4e1c functions in a novel pathway.  Deletion of eif4e1c in zebrafish caused growth deficits and impaired survival in juveniles. Mutants surviving to adulthood had fewer cardiomyocytes, while also showing reduced proliferative responses to cardiac injury. Ribosome profiling of mutant hearts demonstrated changes in translation efficiency of mRNA for genes known to regulate cardiomyocyte proliferation. Although eif4e1c is expressed in many tissues and is the predominant cap-binding initiation homolog in embryos, its disruption had most notable impact on the heart and at juvenile stages.  Our findings reveal context-dependent requirements for translation initiation regulators during heart regeneration.

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The translation initiation factor homolog eif4e1c regulates cardiomyocyte metabolism and proliferation during heart regeneration.

Project description:The eIF4E family of translation initiation factors bind 5' methylated caps and act as the limiting step for mRNA translation. The canonical eIF4E1A is required for cell viability, yet other related eIF4E families exist and are utilized in specific contexts or tissues. Here, we describe a family called Eif4e1c, for which we find roles during heart development and regeneration in zebrafish. The Eif4e1c family is present in all aquatic vertebrates but is lost in all terrestrial species. A core group of amino acids shared over 500 million years of evolution forms an interface along the protein surface, suggesting that Eif4e1c functions in a novel pathway. Deletion of eif4e1c in zebrafish caused growth deficits and impaired survival in juveniles. Mutants surviving to adulthood had fewer cardiomyocytes and reduced proliferative responses to cardiac injury. Ribosome profiling of mutant hearts demonstrated changes in translation efficiency of mRNA for genes known to regulate cardiomyocyte proliferation. Although eif4e1c is broadly expressed, its disruption had most notable impact on the heart and at juvenile stages. Our findings reveal context-dependent requirements for translation initiation regulators during heart regeneration.

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Codon usage and protein length-dependent feedback from translation elongation to translation initiation and kinetics

Project description:In yeast and mammals, activated GCN2 can phosphorylate its substrate eIF2α, which is a part of the eIF2-GTP-Met-tRNAiMet ternary complex. The eIF2α phosphorylation blocks the ternary complex formation and therefore inhibits translation initiation. Meanwhile, GCN2 activation associates with ribosomes and some translation elongation factors such as eEF1A. In Neurospora crassa, the homolog of GCN2 is CPC-3. Ribosome profiling and accompanying RNA-seq experiments in this project were used to explore the effects of CPC-3 on translation kinetics. Here we show that poor codon usage of mRNAs with long CDS preferentially causes CPC-3 activation, which in turn suppresses the translation initiation and elongation in both codon usage and CDS length dependent manner.

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Deep sequencing reveals mRNA recruitment in translation initiation

Project description:We studied the initiation signals located in the translational initiation region (TIR) and identified the role for recognition of the initiation signals in each individual stage during formation of the initiation complexes. Sequencing the randomized mRNA libraries captured by translation initiation complexes

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α-Ketoglutarate Promotes Cardiomyocyte Proliferation and Heart Regeneration after Myocardial Infarction

Project description:The neonatal mammalian heart is capable of substantial regeneration following injury through cardiomyocyte proliferation. However, this regenerative capacity is lost by postnatal (P) day 7. How to stimulate the adult cardiomyocyte to re-enter the cell cycle is still unknown. Accumulating evidence suggests that cardiomyocyte proliferation depends on its metabolic state. Due to the tight connection between the tricarboxylic acid cycle (TCA) and cell proliferation, we analyzed the TCA metabolites between P0.5 and P7 mouse hearts and found that α-ketoglutarate (α-KG) ranked first among the decreased metabolites. The intraperitoneal injection of exogenous α-KG extended the window of cardiomyocyte proliferation during heart development and promoted heart regeneration after myocardial infarction (MI) by inducing adult cardiomyocyte proliferation. This was confirmed in Ogdh-siRNA-treated mice with increased α-KG levels. Mechanistically, α-KG activates Jmjd3, a histone lysine demethylase, that decreases H3K27me3 expression and deposition of H3K4me3 at the promoters of cell cycle and structural maturation genes in cardiomyocytes. Our present study shows that α-KG promotes cardiomyocyte proliferation by Jmjd3-dependent demethylation and inactivation of H3K27me3 andH3K4me3, which is a potential therapeutic approach for treating MI and heart failure.

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Synonymous codon usage regulates translation initiation

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Glucose depletion inhibits translation initiation in yeast - transcription profiling

Project description:This is a transcription profiling study on yeast undergoing glucose depletion. It reveals that glucose depletion inhibits translation initiation in a mechanism involving eIF4A loss and 48S pre-initiation complex accumulation, while the pentose phosphate pathway is co-ordinately up-regulated

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Comprehensive profiling of translation initiation in influenza-virus infected cells

Project description:Cellular stress is often accompanied by non-canonical initiation of translation at alternate start codons in mammalian cells. Here we systematically investigate the extent and impact of alternate translation initiation in the context of influenza virus infection. We use ribosome profiling with the initiation inhibitor lactidomycin to experimentally delineate translation initiation sites in a human lung epithelial cell line infected with influenza virus.

2018-05-20 | GSE114636 | GEO

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