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Decoding of translation-regulating entities reveals heterogeneous translation deficiency patterns in cellular senescence

ABSTRACT: Decoding of translation-regulating entities reveals heterogeneous translation deficiency patterns in cellular senescence

PROVIDER: PRJNA933910 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23418160_1.fastq.gz	Fastqsanger.gz
	SRR23418160_2.fastq.gz	Fastqsanger.gz
	SRR23418161_1.fastq.gz	Fastqsanger.gz
	SRR23418161_2.fastq.gz	Fastqsanger.gz
	SRR23418162_1.fastq.gz	Fastqsanger.gz

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Decoding of translation-regulating entities reveals heterogeneous translation deficiency patterns in cellular senescence

Project description:Cellular senescence constitutes a generally irreversible proliferation barrier, accompanied by macromolecular damage and metabolic rewiring. Several senescence types have been identified based on the initiating stimulus, such as replicative (RS), stress-induced (SIS) and oncogene-induced senescence (OIS). Reduced protein synthesis is considered a senescence hallmark, but whether this trait pertains to various senescence subtypes and if distinct molecular mechanisms are involved remain largely unknown. Here, we analyze large published or experimentally produced RNA-seq and Ribo-seq datasets to determine whether major translation-regulating entities such as ribosome stalling, the presence of uORFs/dORFs and IRES elements may differentially contribute to translation deficiency in senescence subsets. We show that translation-regulating mechanisms may not be directly relevant to RS, however uORFs are significantly enriched in SIS. Interestingly, ribosome stalling, uORF/dORF patterns and IRES elements comprise predominant mechanisms upon OIS, strongly correlating with Notch pathway activation. Our study provides for the first time evidence that major translation dysregulation mechanisms/patterns occur during cellular senescence, but at different rates depending on the stimulus type. The degree at which those mechanisms accumulate directly correlates with translation deficiency levels. Our thorough analysis contributes to elucidating crucial and so far unknown differences in the translation machinery and ribosome biogenesis between senescence subsets.

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Decoding of translation-regulating entities reveals heterogeneous translation deficiency patterns in cellular senescence.

Project description:Cellular senescence constitutes a generally irreversible proliferation barrier, accompanied by macromolecular damage and metabolic rewiring. Several senescence types have been identified based on the initiating stimulus, such as replicative (RS), stress-induced (SIS) and oncogene-induced senescence (OIS). These senescence subtypes are heterogeneous and often develop subset-specific phenotypes. Reduced protein synthesis is considered a senescence hallmark, but whether this trait pertains to various senescence subtypes and if distinct molecular mechanisms are involved remain largely unknown. Here, we analyze large published or experimentally produced RNA-seq and Ribo-seq datasets to determine whether major translation-regulating entities such as ribosome stalling, the presence of uORFs/dORFs and IRES elements may differentially contribute to translation deficiency in senescence subsets. We show that translation-regulating mechanisms may not be directly relevant to RS, however uORFs are significantly enriched in SIS. Interestingly, ribosome stalling, uORF/dORF patterns and IRES elements comprise predominant mechanisms upon OIS, strongly correlating with Notch pathway activation. Our study provides for the first time evidence that major translation dysregulation mechanisms/patterns occur during cellular senescence, but at different rates depending on the stimulus type. The degree at which those mechanisms accumulate directly correlates with translation deficiency levels. Our thorough analysis contributes to elucidating crucial and so far unknown differences in the translation machinery between senescence subsets.

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Decoding Heterogeneous and Coordinated Tissue Architecture in Glioblastoma Using Spatial Transcriptomics

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Project description:The mammalian oviduct is a dynamic organ and the venue of important events leading to the establishment of pregnancy. Oviductal epithelial cells are involved in direct contact and specific interactions with different self and non-self entities (oocyte, sperm, etc.).The aim of this study was to determine if the oviduct is able to distinguish between different types of non-self-entities. We used an in vitro model to determine genes altered in oviductal epithelial cell (OPEC) in response to the presence of spermatozoa, mammalian somatic cells (red blood cell) or bacteria. We hypothesised that alteration of OPEC expression profile in response to boar spermatozoa (friendly non-self entity), red blood cells (non-pathogenic, non-self entity) and bacteria (pathogenic non-self entity) is indicative of recognition of self and non-self entities by these cells as well as recognition of pathogenic from non-pathogenic non-self entities.

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