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. Author manuscript; available in PMC: 2019 Jul 15.
Published in final edited form as: Dev Biol. 2018 Apr 19;439(2):102–111. doi: 10.1016/j.ydbio.2018.04.012

Figure 5. Loss of Foxd1 results in a broad and selective loss of anterior hypothalamic markers at P0.

Figure 5

A–H; K–B’: In situ hybridization of coronal sections from P0 heterozygote controls and Foxd1 mutant brain. Expression of selective markers of the SCN was either absent or greatly reduced in Foxd1 mutants relative to controls (open arrowheads, A–H, K–P, S, T). Gad67 expression, however, was unaffected (open arrowheads, W, X), as were Th and Trh (open arrowheads, Y–B’), which are expressed in regions of the AH adjacent to the SCN. In sharp contrast to wild-type animals (red dashed outline, I) the majority of Foxd1 mutants showed no evidence of an organized SCN (J). Markers of the PVN were also negatively affected by the loss of Foxd1 (black arrowheads, K, L, Q, R), as was Sst in the PeVN (open arrowheads, Q, R). The broadly expressed hypothalamic marker Isl1 was strongly reduced in anterior hypothalamus, but not in prethalamus (open arrowheads, U, V). Other prethalamic markers were unaffected (red arrowheads, M, N, Q, R). C’: Schematic summarizing developmental defects in the anterior hypothalamus. Expression of anterior hypothalamic markers was either reduced (down arrow) or unaffected (−). (Number of animals analyzed: Lhx1=3; Isl1=4; Sst=10; Gad67=7; AVP=6; Vipr2=3; Rorb=5; Trh=4; Rora=1; Emx2=1; Th=2; Six3=1; Vax1=1)