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ER, mitochondria and ISR regulation by mt-HSP70 and ATF5 upon procollagen misfolding (proximal tibia srRNASeq)

ABSTRACT: ER, mitochondria and ISR regulation by mt-HSP70 and ATF5 upon procollagen misfolding (proximal tibia srRNASeq)

PROVIDER: PRJNA866524 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR20862647.fastq.gz	Fastqsanger.gz
	SRR20862648.fastq.gz	Fastqsanger.gz
	SRR20862649.fastq.gz	Fastqsanger.gz
	SRR20862650.fastq.gz	Fastqsanger.gz
	SRR20862651.fastq.gz	Fastqsanger.gz

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ER, mitochondria and ISR regulation by mt-HSP70 and ATF5 upon procollagen misfolding (E18.5 femur and tibia)

Project description:ER, mitochondria and ISR regulation by mt-HSP70 and ATF5 upon procollagen misfolding (E18.5 femur and tibia)

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ER, mitochondria and ISR regulation by mt-HSP70 and ATF5 upon procollagen misfolding (proximal tibia srRNASeq)

Project description:We used spatially resolved RNA sequencing (srRNA-seq) to identify trabecular osteoblast cell stress response pathway to misfolding of type I procollagen with Gly610->Cys substitution in the triple helical region of alpha2(I) chain (trabecular region of proximal tibia adjacent to the growth plate).

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ER, mitochondria and ISR regulation by mt-HSP70 and ATF5 upon procollagen misfolding (E18.5 femur and tibia)

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ER, mitochondria and ISR regulation by mt-HSP70 and ATF5 upon procollagen misfolding (primary cells)

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ER, mitochondria and ISR regulation by mt-HSP70 and ATF5 upon procollagen misfolding (P5 parietal bone)

Project description:ER, mitochondria and ISR regulation by mt-HSP70 and ATF5 upon procollagen misfolding (P5 parietal bone)

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ER, mitochondria and ISR regulation by mt-HSP70 and ATF5 upon procollagen misfolding (primary cells)

Project description:We used bulk RNA sequencing (bulk RNAseq) in primary osteoblast cultures to validate scRNASeq and srRNASeq findings on osteoblast cell stress response pathway to misfolding of type I procollagen with Gly610->Cys substitution in the triple helical region of alpha2(I) chain.

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ER, mitochondria and ISR regulation by mt-HSP70 and ATF5 upon procollagen misfolding (P5 parietal bone)

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ER, Mitochondria, and ISR Regulation by mt-HSP70 and ATF5 upon Procollagen Misfolding in Osteoblasts.

Project description:Cellular response to protein misfolding underlies multiple diseases. Collagens are the most abundant vertebrate proteins, yet little is known about cellular response to misfolding of their procollagen precursors. Osteoblasts (OBs)-the cells that make bone-produce so much procollagen that it accounts for up to 40% of mRNAs in the cell, which is why bone bears the brunt of mutations causing procollagen misfolding in osteogenesis imperfecta (OI). The present study of a G610C mouse model of OI by multiple transcriptomic techniques provides first solid clues to how OBs respond to misfolded procollagen accumulation in the endoplasmic reticulum (ER) and how this response affects OB function. Surprisingly, misfolded procollagen escapes the quality control in the ER lumen and indirectly triggers the integrated stress response (ISR) through other cell compartments. In G610C OBs, the ISR is regulated by mitochondrial HSP70 (mt-HSP70) and ATF5 instead of their BIP and ATF4 paralogues, which normally activate and regulate ISR to secretory protein misfolding in the ER. The involvement of mt-HSP70 and ATF5 together with other transcriptomic findings suggest that mitochondria might initiate the ISR upon disruption of ER-mitochondria connections or might respond to the ISR activated by a yet unknown sensor.

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Microarray to find ATF5 dependent genes in response to proteasome inhibition

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