Expression profile of P7 control and Lhx2 cKO somatosensory cortex
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE92372 | GEO | 2016/12/15
SECONDARY ACCESSION(S): PRJNA357362
REPOSITORIES: GEO
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Project description:Lhx2 is a retinal progenitor cell transcription factor critical for eye development. We previously reported that conditional inactivation of Lhx2 at the start of mouse retinal neurogenesis disrupted retinal progenitor cell (RPC) proliferation, greatly reduced the RPC pool and altered neurogenic output as indicated by changes in the production of multiple fated precursor populations. To identify genes whose expression levels are dependent on Lhx2 at this stage of development, Lhx2 conditional inactivation was initiated at E11.5 in RPCs with the progenitor Cre driver Hes1CreERT2 and retinal tissue was collected at E15.5 for RNA sequencing. The gene expression profiles of Lhx2 CKO retinas were compared to control (Lhx2 conditional heterozygotes) were compared. Downregulated and upregulated gene expression was observed, with some likely due to direct and indirect regulation by Lhx2 within RPCs and others due to changes in differentiation and the altered neurogenic output.
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Project description:Expression profile of P7 control and Lhx2 cKO somatosensory cortex
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Project description:The Lhx2 transcription factor plays essential roles in morphogenesis and patterning of ectodermal derivatives, as well as in controlling stem cell activity. Lhx2 is expressed in the hair follicle (HF) buds, while in postnatal telogen HFs Lhx2+ cells reside in the stem cell-enriched epithelial compartments (bulge, secondary hair germ) and co-express selected stem cell markers (Sox9, Tcf4 and Lgr5). Lhx2+ cells represent the vast majority of cells in the bulge and secondary hair germ that proliferate in response to skin injury. This is functionally important, since the wound re-epithelialization is significantly retarded in heterozygous Lhx2 knockout (+/-) mice, while anagen onset in the HFs located closely to the wound is accelerated compared to wild-type mice. Cell proliferation in the bulge and the number of Sox9+ and Tcf4+ cells in the HFs closely adjacent to the wound in Lhx2+/- mice are decreased in comparison to wild-type controls, while expression of Lgr5 and cell proliferation in the secondary hair germ are increased. Furthermore, acceleration of wound-induced anagen development in Lhx2+/- mice is inhibited by administration of Lgr5 siRNA. In addition, Chip-on-chip/ChIP-qPCR and reporter assay analyses reveal Sox9, Tcf4 and Lgr5 as direct Lhx2 targets in keratinocytes. These data strongly suggest that Lhx2 positively regulates Sox9 and Tcf4 in the bulge cells and promotes wound re-epithelization, while it simultaneously negatively regulates Lgr5 in the secondary hair germ and inhibits HF cycling. Thus, Lhx2 operates as a regulator of epithelial stem cell activity during skin response to injury. Chromatin form primary mouse keratinocytes (PMK) was subjected to ChIP analysis with Lhx2 antibody; input and ChIP DNA were labelled with Cy3 and Cy5 respectivly and used form Nimblegen MM8 Mouse Promoter Array
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