Abstract
In the epidermis of mice lacking transcription factor nuclear factor-kappa B (NF-κB) activity, primary hair follicle (HF) pre-placode formation is initiated without progression to proper placodes. NF-κB modulates WNT and SHH signaling at early stages of HF development, but this does not fully account for the phenotypes observed upon NF-κB inhibition. To identify additional NF-κB target genes, we developed a novel method to isolate and transcriptionally profile primary HF placodes with active NF-κB signaling. In parallel, we compared gene expression at the same developmental stage in NF-κB-deficient embryos and controls. This uncovered novel NF-κB target genes with potential roles in priming HF placodes for down-growth. Importantly, we identify Lhx2 (encoding a LIM/homeobox transcription factor) as a direct NF-κB target gene, loss of which replicates a subset of phenotypes seen in NF-κB-deficient embryos. Lhx2 and Tgfb2 knockout embryos exhibit very similar abnormalities in HF development, including failure of the E-cadherin suppression required for follicle down-growth. We show that TGFβ2 signaling is impaired in NF-κB-deficient and Lhx2 knockout embryos and that exogenous TGFβ2 rescues the HF phenotypes in Lhx2 knockout skin explants, indicating that it operates downstream of LHX2. These findings identify a novel NF-κB/LHX2/TGFβ2 signaling axis that is crucial for primary HF morphogenesis, which may also function more broadly in development and disease.
Original language | English |
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Pages (from-to) | 1512-22 |
Number of pages | 11 |
Journal | Development (Cambridge, England) |
Volume | 143 |
Issue number | 9 |
Early online date | 7 Mar 2016 |
DOIs | |
Publication status | Published - 3 May 2016 |
Keywords
- Animals
- Cadherins/metabolism
- Cell Differentiation/genetics
- Cell Movement/genetics
- Embryo, Mammalian/metabolism
- Gene Expression Regulation, Developmental/genetics
- Hair Follicle/embryology
- LIM-Homeodomain Proteins/genetics
- Mice
- Mice, Knockout
- Organ Culture Techniques
- Organogenesis/genetics
- Receptors, Transforming Growth Factor beta/metabolism
- Transcription Factor RelA/genetics
- Transcription Factors/genetics
- Transforming Growth Factor beta2/genetics