Fibroblast Growth Factor Receptors (FGFRs) play crucial roles in promoting dendrite growth and branching during development. In mice, three FGFR genes, Fgfr1, Fgfr2, and Fgfr3, remain expressed in the adult neurogenic niche of the hippocampal dentate gyrus. However, the function of FGFRs in the dendritic maturation of adult-born neurons remains largely unexplored. Here, using conditional alleles of Fgfr1, Fgfr2, and Fgfr3 as well as Fgfr1 alleles lacking binding sites for Phospholipase-Cγ (PLCγ) and FGF Receptor Substrate (FRS) proteins, we test the requirement for FGFRs in dendritogenesis of adult-born granule cells. We find that deleting all three receptors results in a small decrease in proximal dendrite elaboration. In contrast, specifically mutating Tyr766 in FGFR1 (a PLCγ binding site) in an Fgfr2;Fgfr3 deficient background results in a dramatic increase of overall dendrite elaboration, while blocking FGFR1-FRS signaling causes proximal dendrite deficits and, to a lesser extent than Tyr766 mutants, increases distal dendrite elaboration. These findings reveal unexpectedly complex roles for FGFRs and their intracellular mediators in regulating proximal and distal dendrite elaboration, with the most notable role in suppressing distal elaboration through the PLCγbinding site.

成纤维细胞生长因子受体 (FGFRs) 在促进发育过程中的树突生长和分枝方面发挥着至关重要的作用。在小鼠中，三个 FGFR 基因Fgfr1、Fgfr2和Fgfr3仍然在海马齿状回的成年神经源性生态位中表达。然而，FGFRs 在成年神经元树突成熟中的作用在很大程度上仍未被探索。在这里，使用Fgfr1、Fgfr2 和 Fgfr3以及Fgfr1的条件等位基因等位基因缺乏磷脂酶-Cγ (PLCγ) 和 FGF 受体底物 (FRS) 蛋白的结合位点，我们测试了成体颗粒细胞树突形成中对 FGFRs 的需求。我们发现删除所有三个受体会导致近端树突精细化的小幅下降。相反，在 Fgfr2 中的 FGFR1（PLCγ 结合位点）中特异性突变Tyr766；Fgfr3缺乏背景会导致整体树突加工的显着增加，而阻断 FGFR1-FRS 信号会导致近端树突缺陷，并且比 Tyr766 突变体在较小程度上增加远端树突加工。这些发现揭示了 FGFRs 及其细胞内介质在调节近端和远端树突加工中的复杂作用，其中最显着的作用是通过 PLCγ 结合位点抑制远端加工。