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Dkk4 and Eda regulate distinctive developmental mechanisms for subtypes of mouse hair-1

ABSTRACT: Dkk4 transgenic mice in wild-type background showed abnormal hair subtype formation. Gene expression profiling showed significant down regulation of hair follicle-related keratin genes and hair keratin-associated protein genes at E18.5 and P1. Keywords: development or differentiation design,genetic modification design

ORGANISM(S): Mus musculus

PROVIDER: GSE19309 | GEO | 2010/09/03

SECONDARY ACCESSION(S): PRJNA123685

REPOSITORIES: GEO

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Dkk4 and Eda regulate distinctive developmental mechanisms for subtypes of mouse hair-1

Project description:Dkk4 transgenic mice in wild-type background showed abnormal hair subtype formation. Gene expression profiling showed significant down regulation of hair follicle-related keratin genes and hair keratin-associated protein genes at E18.5 and P1. Keywords: development or differentiation design,genetic modification design To define target genes of Dkk4 during hair follicle development, we carried out microarray experiments with mouse back skin samples that from 4 developmental time points including E14.5, E16.5, E18.5 and P1 of wild-type and wild-type background Dkk4 transgenic mice.

2010-09-03 | E-GEOD-19309 | biostudies-arrayexpress

Dkk4 and Eda regulate distinctive developmental mechanisms for subtypes of mouse hair-2

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Dkk4 and Eda regulate distinctive developmental mechanisms for subtypes of mouse hair-2

Project description:Dkk4 transgenic mice in Tabby background lack hair follicle formation. Gene expression profiling showed significant down regulation of Shh pathway genes at E16.5 and E17.5, the secondary hair follicle induction stages. Keywords: development or differentiation design,genetic modification design To define target genes of Dkk4 during secondary hair follicle induction, we carried out microarray experiments with mouse back skin samples that from 2 developmental time points including E16.5 and E17.5 of Tabby and Tabby background Dkk4 transgenic mice.

2010-09-03 | E-GEOD-19312 | biostudies-arrayexpress

Dkk4 and Eda regulate distinctive developmental mechanisms for subtypes of mouse hair

Project description:This SuperSeries is composed of the following subset Series: GSE19309: Dkk4 and Eda regulate distinctive developmental mechanisms for subtypes of mouse hair-1 GSE19312: Dkk4 and Eda regulate distinctive developmental mechanisms for subtypes of mouse hair-2 Refer to individual Series

2010-09-03 | E-GEOD-19364 | biostudies-arrayexpress

Reductively extracted human hair keratin

Project description:Human hair keratin was extracted from hair by a reduction method and analyzed by Matrix-Assisted Laser Desorption Ionization-Time of Flight Mass Spectrometer.

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Dkk4 and Eda regulate distinctive developmental mechanisms for subtypes of mouse hair.

Project description:The mouse hair coat comprises protective "primary" and thermo-regulatory "secondary" hairs. Primary hair formation is ectodysplasin (Eda) dependent, but it has been puzzling that Tabby (Eda(-/y)) mice still make secondary hair. We report that Dickkopf 4 (Dkk4), a Wnt antagonist, affects an auxiliary pathway for Eda-independent development of secondary hair. A Dkk4 transgene in wild-type mice had no effect on primary hair, but secondary hairs were severely malformed. Dkk4 action on secondary hair was further demonstrated when the transgene was introduced into Tabby mice: the usual secondary follicle induction was completely blocked. The Dkk4-regulated secondary hair pathway, like the Eda-dependent primary hair pathway, is further mediated by selective activation of Shh. The results thus reveal two complex molecular pathways that distinctly regulate subtype-based morphogenesis of hair follicles, and provide a resolution for the longstanding puzzle of hair formation in Tabby mice lacking Eda.

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Alopecia areata susceptibility variant in MHC region impacts expressions of genes contributing to hair keratinization and is involved in hair loss

Project description:Background: Alopecia areata (AA) is considered a highly heritable, T-cell-mediated autoimmune disease of the hair follicle. However, no convincing susceptibility gene has yet been pinpointed in the major histocompatibility complex (MHC), a genome region known to be associated with AA as compared to other regions. Methods: We engineered mice carrying AA risk allele identified by haplotype sequencing for the MHC region using allele-specific genome editing with the CRISPR/Cas9 system. Finally, we performed functional evaluations in the mice and AA patients with and without the risk allele. Findings: We identified a variant (rs142986308, p.Arg587Trp) in the coiled-coil alpha-helical rod protein 1 (CCHCR1) gene as the only non-synonymous variant in the AA risk haplotype. Furthermore, mice engineered to carry the risk allele displayed a hair loss phenotype. Transcriptomics further identified CCHCR1 as a novel component interacting with hair cortex keratin in hair shafts. Both, these alopecic mice and AA patients with the risk allele displayed morphologically impaired hair and comparable differential expression of hair-related genes, including hair keratin and keratin-associated proteins (KRTAPs). Interpretation: Our results implicate CCHCR1 with the risk allele in a previously unidentified subtype of AA based on aberrant keratinization in addition to autoimmune events.

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Transcriptional response to aminoglycoside antibiotics in cochlear hair cells at 3 hour

Project description:We purified Atoh1-GFP positive hair cells from organotypic cultures of P1 cochlea 3 hours after 0.5mM gentamicin treatment and performed RNA sequencing to profile the early transcriptional response of hair cells to aminoglycoside antibiotics. Levels of mRNA in gentamicin-treated hair cells (three replicates) were compared to untreated hair cells (three replicates). GFP negative, non-hair cells populations from treated organs were compared to those from untreated organs (three replicates for each condition).

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Transcriptional response to aminoglycoside antibiotics in cochlear hair cells at 3 hour

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