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RNA-seq of full thickness small intestine from Atg16l1 T300A and wildtype littermate mice that were either exposed or not with mainstream cigarette smoking for 6 weeks

ABSTRACT: RNA-seq of full thickness small intestine from Atg16l1 T300A and wildtype littermate mice that were either exposed or not with mainstream cigarette smoking for 6 weeks

PROVIDER: PRJEB20572 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR1949290.fastq.gz	Fastqsanger.gz
	ERR1949291.fastq.gz	Fastqsanger.gz
	ERR1949292.fastq.gz	Fastqsanger.gz
	ERR1949293.fastq.gz	Fastqsanger.gz
	ERR1949284.fastq.gz	Fastqsanger.gz

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RNA-seq of full thickness small intestine from Atg16l1 T300A and wildtype littermate mice that were either exposed or not with mainstream cigarette smoking for 6 weeks

Project description:We found that mainstream cigarette smoking (4 cigarettes/day, 5 days/week for 6 weeks using Kentucky Research Cigarettes 3R4F) resulted in >20% decrease in the percentage of normal Paneth cell population in Atg16l1 T300A mice but showed minimal effect in wildtype littermate control mice, indicating that Atg16l1 T300A polymorphism confers sensitivity to cigarette smoking-induced Paneth cell damage. We performed transcriptional profiling to identify molecular mechanisms associated with Paneth cell defect in Atg16l1 T300A mice exposed to cigarette smoking. Female mice were used at 4-5 weeks of age. Cigarette smoking was performed using smoking chamber with the dosage and schedule as described above. The whole ileum of the mice were harvested for transcriptomic analysis after completing 6 weeks of smoking.

2018-10-31 | E-MTAB-5707 | biostudies-arrayexpress

16S rRNA sequencing of fecal samples from Atg16l1 T300A and wildtype littermate mice that were exposed to mainstream cigarette smoking co-housed with mice from the same genotype but not exposed to cigarette smoking

Project description:We found that mainstream cigarette smoking (4 cigarettes/day, 5 days/week for 2 weeks using Kentucky Research Cigarettes 3R4F) resulted in >20% decrease in the percentage of normal Paneth cell population in Atg16l1 T300A mice but showed minimal effect in wildtype littermate control mice, indicating that Atg16l1 T300A polymorphism confers sensitivity to cigarette smoking-induced Paneth cell damage. We performed cohousing experiments to test if Paneth cell phenotype is horizontally transmissible as is microbiota. Atg16l1 T300A and littermate controls that were exposed to cigarette smoking were used as microbiota donors, and these donor mice were exposed to smoking for 2 weeks prior to cohousing. Separate groups of Atg16l1 T300A and littermate controls that were not exposed to cigarette smoking were used as microbiota recipients. The microbiota recipients were co-housed with microbiota donors of the same genotype for 4 weeks, during this period the donors continued to be exposed to cigarette smoking. Cigarette smoking was performed using smoking chamber with the dosage and schedule as described above. At the end of the experiment, the fecal microbiota composition was analyzed by 16S rRNA sequencing.

2018-10-31 | E-MTAB-5720 | biostudies-arrayexpress

16S rRNA sequencing of fecal samples from Atg16l1 T300A and wildtype littermate mice that were either exposed or not to mainstream cigarette smoking for 6 weeks

2018-10-31 | E-MTAB-5717 | biostudies-arrayexpress

Microarray of laser capture microdissected Paneth cells from Atg16l1 T300A and wildtype littermates mice that were either exposed or not with mainstream cigarette smoking for 6 weeks

Project description:We found that mainstream cigarette smoking (4 cigarettes/day, 5 days/week for 2 weeks using Kentucky Research Cigarettes 3R4F) resulted in >20% decrease in the percentage of normal Paneth cell population in Atg16l1 T300A mice but showed minimal effect wildtype littermate control mice, indicating that Atg16l1 T300A polymorphism confers sensitivity to cigarette smoking-induced Paneth cell damage. We performed transcriptional profiling to identify molecular mechanisms associated with Paneth cell defect in Atg16l1 T300A mice exposed to cigarette smoking. Female mice were used at 4-5 weeks of age. Cigarette smoking was performed using smoking chamber with the dosage and schedule as described above. The Paneth cells of the mice were harvested by laser capture microdissection for transcriptomic analysis after completing 6 weeks of smoking.

2018-10-31 | E-MTAB-6168 | biostudies-arrayexpress

E-MTAB-5707

Project description:RNA-seq of full thickness small intestine from Atg16l1 T300A and wildtype littermate mice that were either exposed or not with mainstream cigarette smoking for 6 weeks

2019-05-14 | E-MTAB-5707 | ExpressionAtlas

16S rRNA sequencing of fecal samples from Atg16l1 T300A and wildtype littermate mice that were either exposed or not to mainstream cigarette smoking for 6 weeks

Project description:16S rRNA sequencing of fecal samples from Atg16l1 T300A and wildtype littermate mice that were either exposed or not to mainstream cigarette smoking for 6 weeks

| PRJEB20611 | ENA

Project description:16S rRNA sequencing of fecal samples from Atg16l1 T300A and wildtype littermate mice that were exposed to mainstream cigarette smoking co-housed with mice from the same genotype but not exposed to cigarette smoking

| PRJEB20612 | ENA

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2023-07-13 | GSE218854 | GEO

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Project description:The ATG16L1-deficient intestinal organoids display increased IFN-I signature.

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The V-ATPase/ATG16L1 axis is controlled by the V1H subunit

Project description:Defects in organellar acidification indicate compromised or infected compartments. Recruitment of the autophagy-related ATG16L1 complex to pathologically de-acidified compartments targets ubiquitin-like ATG8 molecules to perturbed membranes. How this process is coupled to pH gradient disruption is unclear. Here, we reveal a direct role for the V1H subunit of the V-ATPase proton pump in recruiting ATG16L1. The interaction between V1H and ATG16L1 occurs within assembled V-ATPases, but not dissociated V1 complexes. This selectivity allows recruitment to be coupled to changes in V-ATPase assembly that follow pH dissipation. Cells lacking V1H undergo canonical macroautophagy but are unable to recruit ATG16L1 in response to influenza infection, STING activation or ionophore drugs. We identify a loop within V1H that mediates ATG16L1 binding, which is absent in a neuronal isoform of V1H. Thus, V1H controls ATG16L1 recruitment in response to proton gradient dissipation, suggesting that the V-ATPase acts autonomously as a cell-intrinsic damage sensor.

2025-01-30 | PXD052945 | Pride

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