{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,16]],"date-time":"2026-10-16T06:21:43Z","timestamp":1792131703077,"version":"4.4.0"},"reference-count":79,"publisher":"Society for Neuroscience","issue":"9","license":[{"start":{"date-parts":[[2012,8,29]],"date-time":"2012-08-29T00:00:00Z","timestamp":1346198400000},"content-version":"vor","delay-in-days":182,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc-sa\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J. Neurosci."],"published-print":{"date-parts":[[2012,2,29]]},"abstract":"<jats:p><jats:italic>Foxg1<\/jats:italic>, formerly<jats:italic>BF-1<\/jats:italic>, is expressed continuously in the postnatal and adult hippocampal dentate gyrus (DG). This transcription factor (TF) is thought to be involved in Rett syndrome, which is characterized by reduced hippocampus size, indicating its important role in hippocampal development. Due to the perinatal death of<jats:italic>Foxg1<\/jats:italic><jats:sup>\u2212\/\u2212<\/jats:sup>mice, the function of<jats:italic>Foxg1<\/jats:italic>in postnatal DG neurogenesis remains to be explored. Here, we describe the generation of a<jats:italic>Foxg1<\/jats:italic><jats:sup>fl\/fl<\/jats:sup>mouse line.<jats:italic>Foxg1<\/jats:italic>was conditionally ablated from the DG during prenatal and postnatal development by crossing this line with a<jats:italic>Frizzled9<\/jats:italic>-CreER<jats:sup>TM<\/jats:sup>line and inducing recombination with tamoxifen. In this study, we first show that disruption of<jats:italic>Foxg1<\/jats:italic>results in the loss of the subgranular zone and a severely disrupted secondary radial glial scaffold, leading to the impaired migration of granule cells. Moreover, detailed analysis reveals that<jats:italic>Foxg1<\/jats:italic>may be necessary for the maintenance of the DG progenitor pool and that the lack of<jats:italic>Foxg1<\/jats:italic>promotes both gliogenesis and neurogenesis. We additionally show that<jats:italic>Foxg1<\/jats:italic>may be required for the survival and maturation of postmitotic neurons and that<jats:italic>Foxg1<\/jats:italic>may be involved in Reelin signaling in regulating postnatal DG development. Last, prenatal deletion of<jats:italic>Foxg1<\/jats:italic>suggests that it is rarely involved in the migration of primordial granule cells. In summary, we report that<jats:italic>Foxg1<\/jats:italic>is critical for DG formation, especially during early postnatal stage.<\/jats:p>","DOI":"10.1523\/jneurosci.5240-11.2012","type":"journal-article","created":{"date-parts":[[2012,3,1]],"date-time":"2012-03-01T00:58:28Z","timestamp":1330563508000},"page":"2931-2949","source":"Crossref","is-referenced-by-count":91,"title":["<i>Foxg1<\/i>Has an Essential Role in Postnatal Development of the Dentate 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