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Molecular consequences of Dlx3 deletion by tamoxifen inducible K14 Cre in adult mouse epidermis (P42-P46) as determined by RNASeq analysis

ABSTRACT: Molecular consequences of Dlx3 deletion by tamoxifen inducible K14 Cre in adult mouse epidermis (P42-P46) as determined by RNASeq analysis

PROVIDER: PRJNA407977 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6051650.fastq.gz	Fastqsanger.gz
	SRR6051660.fastq.gz	Fastqsanger.gz
	SRR6051641.fastq.gz	Fastqsanger.gz
	SRR6051651.fastq.gz	Fastqsanger.gz
	SRR6051661.fastq.gz	Fastqsanger.gz

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Molecular consequences of Dlx3 deletion by tamoxifen inducible K14 Cre in adult mouse epidermis (P42-P46) as determined by RNASeq analysis

Project description:DLX3 is a homeodomain transcription factor involved in epidermal and hair follicle differentiation. Epidermal specific deletion of DLX3 leads to IL17 related inflammation. However, the downstream signals from DLX3-deficient keratinocytes that initiates IL17 associated inflammation is not well-characterized. Therefore we performed acute Dlx3 deletion to identify the initial molecular changes causing the skin inflammatory reponse and tried to rescue the immune phenotype by STAT3 inhibitor treatment (Cryptotanshinone). In this study, we compared the epidermal and dermal transcriptome from Dlx3 wild-type (WT) and K14CreERT;DLX3 fl/fl (icKO).

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Molecular consequences of Dlx3 deletion in mouse enamel organ as determined by RNASeq analysis

Project description:DLX3 is a homeodomain transcription factor involved in ameloblast differentiation and enamel formation. Mutations in DLX3 in human lead to defects in enamel. However, the downstream targets of Dlx3 transcriptional activity in the enamel organ have not been identified yet. In this study, we compared the transcriptome of enamel organs where Dlx3 has been deleted to control tissues. Total RNA was extracted from enamel organs (mandibular incisors) from Dlx3-WT (N=4) and Dlx3-K14cKO (N=4) mice at P10. cDNA libraries were generated using NEBnext and NuGen kits. Sequencing was performed on the HiSeq2000.

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Molecular consequences of Dlx3 deletion in mouse enamel organ as determined by RNASeq analysis

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Molecular consequences of Dlx3 deletion in mouse enamel organ as determined by microarray analysis

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DLX3 binding sites in rat enamel organ

Project description:DLX3 is a homeodomain transcription factor involved in amelogenesis. Mutations in DLX3 in human lead to Tricho-Dento-Osseous syndrome featuring enamel hypoplasia and hypomineralization. Here we investigated the distribution of DLX3 DNA binding sites in rat enamel organ using ChIP-seq.

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DLX3 binding sites in Supabasal Keratinocytes

Project description:DLX3 is a homeodomain transcription factor involved in epidermal differentiation. Here we investigated the distribution of DLX3 DNA binding sites in suprabasal differentiating keratinocytes using ChIP-seq.

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Dlx3 Regulates Lifr and Chrdl1 Expression in Mouse Embryonic Stem Cell Differentiation

Project description:Dlx3 over-expression in mouse embryonic fibroblasts changed the expression level of numerous genes involved in osteogenesis and embryonic stem cell-related pathways as revealed by microarray analysis. From the list of Dlx3 modulated genes we focused our attention on the study of two candidates, Lifr and Chrdl1. Chromatin immunoprecipitation demonstrated the recruitment of Dlx3 transcription factor to the promoters of Lifr and Chrdl1, and luciferase assays confirmed the role of Dlx3 in the regulation of Lifr expression. Over-expression of Dlx3 in mouse embryonic stem cells stimulated Lifr and Chrdl1 expression and inhibited expression of Id proteins and Bmp4. We show that Dlx3 increases the expression of both soluble and transmembrane forms of Lifr. Soluble Lifr may regulate extracellular Lif levels via solution binding, while transmembrane Lifr mediates the signal transduction pathway. The data suggests that Dlx3 may be involved in stem cell differentiation in a dosage dependent way through its interaction with Lifr and with Chrdl1, a known antagonist of Bmp4. We speculate that Dlx3 may also be involved in osteoblast differentiation through interactions involving Lifr, Bmp, and Id proteins and signaling via the JAK/STAT and MAPK pathways. In summary, our data suggests that Dlx3 proteins play a significant role in a highly tuned network in early embryogenesis. Keywords: treated vs.untreated Stable and Transient transfection of Dlx3 in MEF. Total of 4 hybridizations including biological replicates.

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Dlx3 Regulates Lifr and Chrdl1 Expression in Mouse Embryonic Stem Cell Differentiation

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