The abstract is read at the publisher; the summary is JClub's.
LHX2-driven DACH1 expression programs basal radial glia expansion in the primate neocortex, and DACH1 loss in human progenitors impairs bRG production.
- Why it matters: Primate neocortex development depends on an expanded progenitor pool, but the regulatory innovations that control basal radial glia output and downstream circuitry are unclear.
- What they did: Comparative transcriptomics in developing human versus mouse neocortical cells highlighted DACH1 in human neurogenic RGs; primate ESCs and mouse models tested an LHX2–DACH1–miR-215-5p regulatory program and a primate-evolved enhancer.
- The result: DACH1 loss in human progenitors reduces bRG production and shifts output toward corticospinal neurons, while ectopic DACH1 in rodent neocortex induces bRG and callosal neurons; enhancer gain in mice promotes bRG and enhancer removal in primates impairs bRG.
The findingWhy it mattersWhat they didThe result
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