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Chunk #23 — Results — Deleting Zfhx1b in SVZ of the MGE Using DlxI12b-Cre Phenocopies Loss of Zfhx1b function in the VZ (Nkx2.1-Cre) — Postnatal Analysis of cortical and striatal interneuron phenotypes in Nkx2.1-Cre;Zfhx1b mutants

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Dlx1&2-dependent expression of Zfhx1b (Sip1, Zeb2) regulates the fate switch between cortical and striatal interneurons.
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At P15 the number of mutant cells (EGFP+) was roughly the same as in controls, and they were evenly dispersed within the striatum, lacking the cell clusters and ectopia (striatal and caudal amygdala) that were apparent at younger ages (Figure 4M-4M’, 4T). The elimination of the excess mutant striatal cells appears to occur through apoptosis, which is robust at P0 (expression of activated cleaved-caspase 6), particularly in the ectopia (Figure S4C-S4C’).