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Stool-derived 16s rRNA V4 sequencing from inducible intestinal-epithelium-LSD1-cKO mice (Villin-CreERT2+ Lsd1fl/fl (icKO)) against WT (Villin-CreERT2+ Lsd1fl/+ (icKO)) controls (before and 1-6 weeks after tamoxifen treatment)

ABSTRACT: Stool-derived 16s rRNA V4 sequencing from inducible intestinal-epithelium-LSD1-cKO mice (Villin-CreERT2+ Lsd1fl/fl (icKO)) against WT (Villin-CreERT2+ Lsd1fl/+ (icKO)) controls (before and 1-6 weeks after tamoxifen treatment)

PROVIDER: PRJEB59925 | ENA |

REPOSITORIES: ENA

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			Action	DRS
		Other
	ERR10892000_1.fastq.gz	Fastqsanger.gz
	ERR10892000_2.fastq.gz	Fastqsanger.gz
	ERR10892001_1.fastq.gz	Fastqsanger.gz
	ERR10892001_2.fastq.gz	Fastqsanger.gz

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Stool-derived 16s rRNA V4 sequencing from inducible intestinal-epithelium-LSD1-cKO mice (Villin-CreERT2+ Lsd1fl/fl (icKO)) against WT (Villin-CreERT2+ Lsd1fl/+ (icKO)) controls (before and 1-6 weeks after tamoxifen treatment)

Project description:Upon tamoxifen induced recombination, Villin-CreERT2+ Lsd1fl/fl (icKO) mice develop an immature intestinal epithelium characterized by an incomplete differentiation of enterocytes and secretory lineages, reduced number of goblet cells and a complete loss of Paneth cells. The main goal of this experiment was to test whether maturation of intestinal epithelium affects microbiota establishment and development. In addition, this loss of differentiated cell types after Lsd1 recombination is gradual and dependent on renewal times of each specific cell type (i.e. enterocytes take less than a week to be fully replenished while Paneth cells cycle around every 4 weeks). Hence by collecting stool from the same mouse at different time points after tamoxifen induced recombination a relationship between loss of particular cell types and changes in bacterial populations can be established. In addition, we wanted to test whether maturation of intestinal epithelium affects microbiota establishment and development

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Project description:Villin-Cre+ Lsd1fl/fl (cKO) mice display an immature intestinal epithelium characterized by an incomplete differentiation of enterocytes and secretory lineages, reduced number of goblet cells and a complete loss of Paneth cells. This experiment aims to elucidate the differences in stool microbial composition derived from WT (Villin-Cre- Lsd1fl/fl) and cKO mice both in adult (2-month-old) and neonatal (14 days postpartum P14) stages. Different timepoints are crucial to understand the role of intestinal maturation in microbiome composition since said maturation is dependent on time-dependent external cues happening at P14-21 (weaning and transition from milk to solid foods).

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The Rax homeoprotein in Müller glial cells is required for homeostasis maintenance of the postnatal mouse retina

Project description:To address the function of Rax in differentiated Müller glial cells, we generated Rax tamoxifen-induced conditional knock-out (Rax iCKO) mice, where Rax can be depleted in mTFP-labeled Müller glial cells upon tamoxifen treatment, by crossing Raxflox/flox mice with Rlbp1-CreERT2 mice and found histological characteristic of reactive gliosis and an enhanced gliosis of Müller glial cells in the Rax iCKO retina under normal and stress conditions, respectively. RNA sequencing using isolated Müller glial cells from the Rax iCKO retina by fluorescence-activated cell sorting demonstrated that reduced expression of suppressor of cytokine signaling-3 (Socs3), whose depletion leads to reactive gliosis in Müller glial cells. Reporter gene assays showed that Rax directly transactivates Socs3 and we observed decreased expression of Socs3 in Müller glial cells of the Rax iCKO retina by immunostaining. Taken together, these results suggest that the Rax homeoprotein suppresses reactive gliosis in Müller glial cells by transactivating Socs3 in vivo. Our results may shed light on the transcriptional regulatory mechanisms underlying Müller glial cell homeostasis.

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