{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,2]],"date-time":"2026-10-02T02:22:46Z","timestamp":1790907766316,"version":"4.1.0"},"reference-count":57,"publisher":"Society for Neuroscience","issue":"2","license":[{"start":{"date-parts":[[2011,7,12]],"date-time":"2011-07-12T00:00:00Z","timestamp":1310428800000},"content-version":"vor","delay-in-days":181,"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":[[2011,1,12]]},"abstract":"<jats:p>Gonadotropin-releasing hormone-1 (GnRH-1) neurons migrate from the nasal placode to the forebrain where they control gonadal function via the hypothalamic\u2013pituitary\u2013gonadal axis. The birth of GnRH-1-expressing neurons is one of the first neurogenic events in the developing nasal placode. By gene expression screening on single GnRH-1 neurons, amyloid precursor binding protein-1 (FE65) was identified in migratory GnRH-1 neurons. FE65 has been shown to modulate \u03b21-integrin dynamics, actin cytoskeleton, cell motility, and FE65\/amyloid precursor protein signaling has been described in neuro\/glial cell fate determination as well as in modulating neurogenesis. Analysis of two mouse lines, one deficient for the 97 kDa FE65 isoform and a second deficient for the 97 and 60 kDa forms of FE65, showed overlapping phenotypes. In both lines, no migratory defects of the GnRH-1 neurons were observed, but a 25% increase in GnRH-1 neuronal number during embryonic development was found. Bromodeoxyuridine birth tracing and spatiotemporal tracking of GnRH-1 cell precursors demonstrated that the lack of the N-terminal portion of FE65, which includes part of the functional nuclear translocation\/gene transcription domain of FE65 (WW domain), extends the timing of GnRH-1 neurogenesis in the developing nasal placode without affecting proliferation of GnRH-1 neuronal progenitors or cell death. The observed changes in the dynamics of GnRH-1 neurogenesis highlight a unique role for the 97 kDa isoform of FE65 and suggest that GnRH-1 cells, which have a short neurogenic window, originate from multipotent progenitors able to generate distinct cell types as GnRH-1 neurogenesis declines in response to environmental changes.<\/jats:p>","DOI":"10.1523\/jneurosci.4698-10.2011","type":"journal-article","created":{"date-parts":[[2011,1,12]],"date-time":"2011-01-12T17:23:23Z","timestamp":1294853003000},"page":"480-491","source":"Crossref","is-referenced-by-count":39,"title":["A Role for FE65 in Controlling GnRH-1 Neurogenesis"],"prefix":"10.1523","volume":"31","author":[{"given":"Paolo 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