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Evolutionarily divergent mTOR remodels translatome for tissue regeneration

ABSTRACT: Evolutionarily divergent mTOR remodels translatome for tissue regeneration

PROVIDER: PRJNA769730 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16264600_1.fastq.gz	Fastqsanger.gz
	SRR16264600_2.fastq.gz	Fastqsanger.gz
	SRR16264601_1.fastq.gz	Fastqsanger.gz
	SRR16264601_2.fastq.gz	Fastqsanger.gz
	SRR16264584_1.fastq.gz	Fastqsanger.gz

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Evolutionarily divergent mTOR remodels translatome for tissue regeneration

Project description:An outstanding mystery in biology is why some species, such as the axolotl, can regenerate tissues whereas mammals cannot1. Here, we demonstrate that rapid activation of protein synthesis is a unique feature of the injury response critical for limb regeneration in the axolotl (Ambystoma mexicanum). By applying polysome sequencing, we identify hundreds of transcripts, including antioxidants and ribosome components that are selectively activated at the level of translation from pre-existing messenger RNAs in response to injury. By contrast, protein synthesis is not activated in response to non-regenerative digit amputation in the mouse. We identify the mTORC1 pathway as a key upstream signal that mediates tissue regeneration and translational control in the axolotl. We discover unique expansions in mTOR protein sequence among urodele amphibians. By engineering an axolotl mTOR (axmTOR) in human cells, we show that these changes create a hypersensitive kinase that allows axolotls to maintain this pathway in a highly labile state primed for rapid activation. This change renders axolotl mTOR more sensitive to nutrient sensing, and inhibition of amino acid transport is sufficient to inhibit tissue regeneration. Together, these findings highlight the unanticipated impact of the translatome on orchestrating the early steps of wound healing in a highly regenerative species and provide a missing link in our understanding of vertebrate regenerative potential.

2023-05-08 | GSE185593 | GEO

Evolutionarily divergent mTOR remodels translatome for tissue regeneration.

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The 40S-LARP1 complex reprograms the cellular translatome upon mTOR inhibition to preserve the protein synthetic capacity

Project description:Ribosomes execute the transcriptional program in every cell. Critical to sustain nearly all cellular activities, ribosome biogenesis requires the translation of ~200 factors of which 80 are ribosomal proteins (RPs). As ribosome synthesis depends on RP mRNAs translation, a priority within the translatome architecture should exist to ensure the preservation of ribosome biogenesis capacity, particularly under adverse growth conditions. Here we show that under critical metabolic constraints characterized by mTOR inhibition, LARP1 complexed with the 40S subunit protects from ribophagy the mRNAs regulon for ribosome biogenesis and protein synthesis, acutely preparing the translatome to promptly resume ribosomes production after growth conditions return permissive. Characterizing the LARP1-protected translatome revealed a set of 5’TOP transcript isoforms other than RPs involved in energy production and in mitochondrial function, among other processes, indicating that the mTOR-LARP1-5’TOP axis acts at the translational level as a primary guardian of the cellular anabolic capacity

2021-10-30 | GSE186779 | GEO

Extensive location bias of the GPCR-dependent translatome via site-selective activation of mTOR

Project description:Extensive location bias of the GPCR-dependent translatome via site-selective activation of mTOR

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Transcriptome and translatome of human regulatory T cells differentiated with TGFbeta and mTOR inhibitor everolimus

Project description:Transcriptome and translatome of human regulatory T cells differentiated with TGFbeta and mTOR inhibitor everolimus

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Next Generation Sequencing Facilitates Quantitative Analysis of Wild Type, genome-edited MTOR(G4448A)-p.C1483Y, and Torin1-treated Wild type Translatomics

Project description:We performed rigorous ribosome profiling in genome-edited cell lines with human MTOR point mutations and Torin1 treated cell lines. By obtaining about 10 million bases of sequence cells, we generated genome-wide translatome and transcriptome data of genome-edited MTOR(G4448A)-p.C1483Y and Torin1 treated cell lines

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Assessment of mTOR-Dependent Translational Regulation of Interferon Stimulated Genes

Project description:Type-I interferon (IFN)-induced activation of the mammalian target of rapamycin (mTOR) signaling pathway has been implicated in translational control of mRNAs encoding interferon-stimulated genes (ISGs). However, mTOR-sensitive translatomes commonly include mRNAs with a 5’ terminal oligopyrimidine tract (TOP), such as those encoding ribosomal proteins, but not ISGs. Because these translatomes were obtained under conditions when ISG expression is not induced, we examined the mTOR-sensitive translatome in human WISH cells stimulated with IFNβ. The mTOR inhibitor Torin1 resulted in a repression of global protein synthesis, including that of ISG products, and translation of all but 3 ISG mRNAs (TLR3, NT5C3A, and RNF19B) was not selectively more sensitive to mTOR inhibition. Detailed studies of NT5C3A revealed an IFN-induced change in transcription start site resulting in a switch from a non-TOP to a TOP-like transcript variant and mTOR sensitive translation. Thus, we show that, in the cell model used, translation of the vast majority of ISG mRNAs is not selectively sensitive to mTOR activity and describe an uncharacterized mechanism wherein the 5’-UTR of an mRNA is altered in response to a cytokine, resulting in a shift from mTOR-insensitive to mTOR-sensitive translation.

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Project description:This experiment performed RNA-seq of transcriptome and translatome (translating mRNA) of Caco-2 cells We extracted transcriptome and translatome from Caco-2 cells and deep sequenced them

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Distinct inhibitory effects on mTOR signaling by ethanol and INK128 in diffuse large B-cell lymphoma

Project description:The mechanistic target of rapamycin, (mTOR) kinase plays a pivotal role in controlling critical cellular growth and survival pathways, and its aberrant induction is implicated in cancer pathogenesis. Therefore, suppression of active mTOR signaling has been of great interest to researchers; several mTOR inhibitors have been discovered to date. Ethanol (EtOH), similar to pharmacologic mTOR inhibitors, has been shown to suppress the mTOR signaling pathway, though in a non-catalytic manner. Despite population studies showing that the consumption of EtOH has a protective effect against hematological malignancies, the mechanisms behind EtOH’s modulation of mTOR activity in cells and its downstream consequences are largely unknown. Here we evaluated the effects of EtOH on the mTOR pathway, in comparison to the active-site mTOR inhibitor INK128, and compared translatome analysis of their downstream effects in diffuse large B-cell lymphoma (DLBCL).

2015-03-03 | GSE62790 | GEO

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