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2022_de Reuver_ADAR1 +/- vs ADAR1 Za/- primary lung fibroblasts

ABSTRACT: Adar +/- vs Adar Za/- primary lung fibroblasts

PROVIDER: PRJEB52610 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR9717702_1.fastq.gz	Fastqsanger.gz
	ERR9717702_2.fastq.gz	Fastqsanger.gz
	ERR9717703_1.fastq.gz	Fastqsanger.gz
	ERR9717703_2.fastq.gz	Fastqsanger.gz
	ERR9717704_1.fastq.gz	Fastqsanger.gz

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Project description:Genome-wide positions of Z-DNA are mapped. ChIP was performed against transiently expressing Flag-Za or Flag-Zaa using Flag antibody in HeLa cells. Za and Zaa ChIP DNA and fragmented genomic DNA were used for sequencing library construction. Each library was sequenced on Illumina GAIIx and HiSeq 2500 and sequenced reads were mapped and normalized.

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RNA-sequencing of lung RNA from mice with compound mutations in ADAR1 and MAVS, ZBP1 or RIPK3.

Project description:The purpose of this study was to examine the role of MAVS, ZBP1 and RIPK3 in the phenotype that develops when ADAR1 activity is impaired, in particular when the Za domain of ADAR1 is mutated. Mice homozygous for a Za domain-mutant allele of Adar1 (Adar1mZa/mZa mice) and mice carrying one mZa and one null Adar1 allele (Adar1-/mZa mice) were compared with control mice that were either wild type or heterozygous for the Adar1 mZa allele (Adar1wt/mZa mice). The effects of MAVS deficiency, RIPK3 deficiency, ZBP1 deficiency or ZBP1 Za domain mutations were assessed by analysing compound mutant mice. Given the early postnatal lethal phenotype that develops in Adar1-/mZa mice, comparisons were made in RNA isolated from lung tissue from newborn mice of each genotype (5 mice per genotype). As Adar1-/mZa mice additionally lacking Mavs or Zbp1 are viable, adult mice (15-20 weeks of age) were also used for several compound mutations as donors of lung tissue.

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Project description:Senescent passage 26 fibroblasts compared to proliferating passage 8 fibroblasts Keywords: Senescent vs. Proliferating

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Cedecea colo strain:ZA

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The phenotype of the most common human ADAR1p150 Za domain mutation P193A in mice is incompletely penetrant

Project description:ADAR1 mediated A-to-I RNA editing is a self/non-self discrimination mechanism for cellular double stranded RNAs. ADAR mutations are one cause of Aicardi-Goutières Syndrome, an inherited paediatric encephalopathy, classed as a “Type I interferonopathy”. The most common ADAR1 mutation is a proline 193 alanine (p.P193A) mutation, mapping to the ADAR1p150 isoform specific Za domain. We report the development of an independent murine P195A knock-in mouse, homologous to the human P193A mutation. The Adar1P195A/P195A mice are largely normal and the mutation is well tolerated. Contrasting with previous reports when the P195A mutation was compounded with an ADAR1 null allele (Adar1P195A/-), we find a partially penetrant phenotype, with approximately half the animals being runted with a shortened lifespan and the remaining animals normal. Severe runting and shortened survival of Adar1P195A/- animals were partly associated with the parental genotype. The P195A mutation is well tolerated in vivo and the loss of MDA5 is sufficient to completely rescue phenotypes in the Adar1P195A/- mice.

2023-02-13 | GSE220628 | GEO

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