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PTK6 regulates secretory cell production and innate immunity in a sex-dependent manner in the intestine

ABSTRACT: PTK6 regulates secretory cell production and innate immunity in a sex-dependent manner in the intestine

PROVIDER: PRJNA1017442 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26060636_1.fastq.gz	Fastqsanger.gz
	SRR26060636_2.fastq.gz	Fastqsanger.gz
	SRR26060637_1.fastq.gz	Fastqsanger.gz
	SRR26060637_2.fastq.gz	Fastqsanger.gz
	SRR26060638_1.fastq.gz	Fastqsanger.gz

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PTK6 regulates secretory cell production and innate immunity in a sex-dependent manner in the intestine

Project description:PTK6 regulates regeneration and repair of the intestinal epithelium. Analysis of publicly available datasets showed Ptk6 is upregulated in tuft cells upon activation of type 2 immunity. We found that disruption of Ptk6 influences gene expression involved in intestinal immune responses. Administration of succinate, which mimics infection and activates tuft cells, revealed PTK6-dependent activation of innate immune responses in male but not female mice. In contrast to wild type and Ptk6-/- female mice, Ptk6-/- male mice do not upregulate innate immunity or differentiation of secretory cell lineages following succinate treatment. Mechanistically, we found PTK6 regulates IL-25 expression and its effector functions, which are required for activation of type 2 innate immunity only in male mice. In patients with Crohn’s disease, PTK6 is upregulated in tuft cells in noninflamed regions of intestine. These data highlight roles for PTK6 in regulating sex differences in intestinal innate immunity and provide insight into the regulation of IL-25.

2024-08-01 | GSE243229 | GEO

Phospho-regulation of Atoh1 is required for plasticity of secretory progenitors and tissue regeneration[intestine]

Project description:To define Atoh1 secretory signature, transcriptional profiling of secretory cells was performed. The expression profile of Atoh1+ cells from Atoh1(WT)CreERT2 R26RtdTom mice was determined by comparing tdTom+ (secretory) and tdTom- (absorptive) cells to define the baseline pro-secretory signature for small intestine (SI).

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Phospho-regulation of Atoh1 is required for plasticity of secretory progenitors and tissue regeneration [colon]

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Phospho-regulation of Atoh1 is required for plasticity of secretory progenitors and tissue regeneration[intestine]

Project description:Phospho-regulation of Atoh1 is required for plasticity of secretory progenitors and tissue regeneration[intestine]

| PRJNA474753 | ENA

Phospho-regulation of Atoh1 is required for plasticity of secretory progenitors and tissue regeneration [bulk RNA-seq]

Project description:To compare secretory signatures of wildtype and mutant mice, the transcription profiles of tdTom+ cells from Atoh1(WT)CreERT2 R26RtdTom and Atoh1(9S/T-A)CreERT2 R26RtdTom mice were generated. The profiles were obtained for both small intestine (SI) and colon.

2018-08-06 | GSE115367 | GEO

Transcriptome of human odontoblast, pre-secretory ameloblast and secretory ameloblast

Project description:The goal of the study was to characterize the whole genome transcriptome profiles of human ameloblasts and odontoblasts, evaluate molecular pathways and advance our knowledge of the human tooth development. We found that during primary tooth formation, odontoblasts expressed 14,802 genes, presecretory ameloblasts 15,179 genes and secretory ameloblasts 14,526 genes. Four human fetuses were obtained at ages 15-20 weeks gestation, immediately placed on ice and the tooth buds dissected from the jaws, placed in RNAlater and refrigerated at 4C for 1-4 weeks to allow decalcification by EDTA. The tissue was then frozen and stored at -80C. The tissue was sectioned at -35C at a thickness of 7 microns. These sections were used for laser capture microdissection (LCM) to isolate the human odontoblasts and ameloblasts in different stages of enamel formation, using static image settings. In total, 4 odontoblast, 4 pre-secretory ameloblast and 4 secretory ameloblast pooled samples were used for RNA extraction and microarray analysis.

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PTK6 domain mutants modulates action in Triple-negative breast cancer

Project description:Protein tyrosine kinase 6 (PTK6; also called Brk) is overexpressed in 86% of breast cancer patients; high PTK6 expression predicts poor outcome. We reported PTK6 induction by HIF/GR complexes in response to either cellular or host stress. However, PTK6-driven signaling events in the context of TNBC remain undefined. In a mouse model of TNBC, manipulation of PTK6 levels (i.e. via knock-out or add-back) had little effect on primary tumor volume but altered lung metastasis. To delineate the mechanisms of PTK6 downstream signaling, we created kinase-dead (KM) and kinase-intact domain structure mutants of PTK6 via in frame deletions of the N-terminal SH3 or SH2 domains. While the PTK6 kinase domain contributed to soft-agar colony formation, PTK6 kinase activity was entirely dispensable for cell migration. Specifically, TNBC models expressing a PTK6 variant lacking the SH2 domain (SH2-del PTK6) were unresponsive to growth factor-stimulated cell motility relative to SH3-del, KM or wild-type PTK6 controls. Reverse phase protein array (RPPA) revealed that while intact PTK6 mediates spheroid formation via p38 MAPK signaling, the SH2 domain of PTK6 limits this biology, and instead mediates TNBC cell motility via activation of the RhoA and/or AhR signaling pathways. Inhibition of RhoA and/or AhR blocked TNBC cell migration as well as the branching/invasive morphology of PTK6+/AhR+ primary breast tumor tissue organoids. Inhibition of RhoA also enhanced paclitaxel cytotoxicity in TNBC cells, including in a taxane-refractory TNBC model. Together, these studies reveal that the SH2-domain of PTK6 is a potent effector of advanced cancer phenotypes in TNBC and identify RhoA and AhR as novel therapeutic targets in PTK6+ breast tumors.

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Altered mucosal homeostasis in mice lacking secretory antibodies

Project description:The mammalian gut is inhabited by a large and complex microbial community that lives in a mutualistic relationship with its host. Innate and adaptive mucosal defense mechanisms ensure a homeostatic relationship with this commensal microbiota. Secretory antibodies are generated from the active polymeric Ig receptor (pIgR)-mediated transport of IgA and IgM antibodies to the gut lumen and form the first line of adaptive immune defense of the intestinal mucosa. We probed mucosal homeostasis in pIgR knockout (KO) mice, which lack secretory antibodies. We found that in pIgR KO mice, colonic epithelial cells, the cell type most closely in contact with intestinal microbes, differentially expressed (>2-fold change) more than 200 genes compared with wild type mice, and upregulated the expression of anti-microbial peptides in a commensal-dependent manner. Detailed profiling of microbial communities based on 16S rRNA genes revealed differences in the commensal microbiota between pIgR KO and wild type mice. Furthermore, we found that pIgR KO mice showed increased susceptibility to dextran sulfate sodium (DSS)-induced colitis, and that this was driven by their conventional intestinal microbiota. In conclusion, secretory antibodies or the pIgR itself are required to maintain a stable commensal microbiota. In the absence of these humoral effector components, gut homeostasis is disturbed and the outcome of colitis significantly worsened. 4 groups: wild type mice treated with antibiotic (5 replicates), wild type mice left untreated (5 replicates), pIgR KO mice treated with antibiotic (6 replicates), and pIgR KO mice left untreated (6 replicates).

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Secretory MPP3 reinforce myeloid differentiation trajectory and amplify myeloid cell production

Project description:Hematopoietic stem cells (HSC) and downstream lineage-biased multipotent progenitors (MPP) tailor blood production and control myelopoiesis on demand. However, a precise resolution of myeloid differentiation trajectories and cellular heterogeneity in various MPP populations and understanding of their role in controlling myeloid cell production remains largely lacking. Here, we analyze that myeloid-biased MPP3 are functionally and molecularly heterogenous, with a distinct subset of myeloid-primed secretory cells with high endoplasmic reticulum (ER) volume.

2021-08-18 | GSE181902 | GEO

intestine

Project description:intestine Raw sequence reads

| PRJNA1085050 | ENA