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Expression profiling experiment on Pkd1-mutant mice and mice induced with nephrotoxin DCVC

ABSTRACT: Expression profiling experiment on Pkd1-mutant mice and mice induced with nephrotoxin DCVC

PROVIDER: PRJEB19240 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR1811850.fastq.gz	Fastqsanger.gz
	ERR1811860.fastq.gz	Fastqsanger.gz
	ERR1811851.fastq.gz	Fastqsanger.gz
	ERR1811861.fastq.gz	Fastqsanger.gz
	ERR1811852.fastq.gz	Fastqsanger.gz

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Expression profiling experiment on Pkd1-mutant mice and mice induced with nephrotoxin DCVC

Project description:To analyze the expression profile of polycystic kideny disease, we generate RNASeq data on Pkd1-mutant mice.RNA sequencing was done on 5 Wild-type (Wt) mice and kidneys of 4 iKsp-Pkd1del mice with gene disruption at the age of 38-40 days (Mutant). Mutant mice, sacrificed 84 days later, had moderate cystic disease. To analyze the expression profiles of injury repair, renal injury was induced one week after tamoxifen administration by a single i.p. injection of S-(1,2-dichlorovinyl)-L-cysteine (DCVC) (15mg/kg). Mice were sacrificed at determined time points (1,2, 5,10 and 24 weeks after DCVC injection). RNA sequencing was performed on the DCVC injected Wt mice sacrificed at 1, 2 and 5 weeks after DCVC (4 mice per each time point).

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Project description:The Pkd1 gene was inactivated by tamoxifen at postnatal day 30 (P30) to generate a chronic-onset conditional Pkd1 gene knockout mouse model. Without any intervention, micro cysts could be detected adjacent to renal medulla-corticomedullary junction in Pkd1-/- mice until P180 and cystic phenotype is severe at P300. However, under dehydration situation, the cyst growth was more accelerated and progressive. The dehydration protocol resulted in Pkd1-/- mice varying degrees of sweating and weight loss. Mice that were not provided water during the day (water at night (D-WAN)) and mice that had access to water during the day (water all time (D-WAT)) showed significantly more weight loss compared with the control Pkd1-/- mice, although they drank more water at night. Interestingly, although D-WAN Pkd1-/- mice and D-WAT Pkd1-/- mice lost approximately body weights after one-day dehydration, while cyst enlargement and renal dysfunction was much more severe in the D-WAN Pkd1-/- mice after two-month intervention.

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Project description:Somatic mutations in non-malignant tissues are selected for because they confer increased clonal fitness, however, it is uncertain if these clones can benefit organ health. Here, ultra-deep targeted sequencing of 150 liver samples from 30 chronic liver disease patients revealed recurrent somatic mutations. PKD1 mutations were observed in 30% of patients, whereas they were only detected in 1.3% of hepatocellular carcinomas (HCCs). To interrogate tumor suppressor functionality, we perturbed PKD1 in two HCC cell lines and six in vivo models, in some cases showing that PKD1 loss protected against HCC, but in most cases showing no impact. However, Pkd1 haploinsufficiency accelerated regeneration after partial hepatectomy. We tested Pkd1 in fatty liver disease, showing that Pkd1 loss was protective against steatosis and glucose intolerance. Mechanistically, Pkd1 loss selectively increased mTOR signaling without SREBP activation. In summary, PKD1 mutations in cirrhotic livers exert adaptive functionality without increasing transformation risk.

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Project description:Expression profiling experiment on Pkd1-mutant mice and mice induced with nephrotoxin DCVC

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