Enriched expression of a Rorα-driven marker in the SCN in RorαCre;R26R mice. (A) Ventral view of a whole brain (magnified view on the right) of adult RorαCre;R26R shows LacZ staining of the SCN. (B) Coronal section through the mid-SCN region (scale bar, 1 mm) and the magnified view of the SCN (scale bar, 100 µm) showing LacZ expression or (C) alkaline phosphatase expression in RorαCre;Z/AP mice. (D) qRT-PCR estimate of Lhx1 expression in the SCN (mean +s.e.m, n = 5). (E) Normal SCN innervation of the retinal ganglion cells in the WT mice as revealed by monocular injection of CTB-conjugated fluorescent marker is intact in (F) Lhx1SCN−KO mice. A 1 hr light pulse at CT16 causes (G) upregulation of light-induced genes (Per1, Per2, cFos, JunB), while (H) the light-suppressed transcripts (Lhx1, Vip, Avpr1a) in the WT SCN show reduced expression in the Lhx1SCN-KO mice. Mice were in DD for 2 days before the light pulse. Representative actograms of (I) RorαCre/Cre, (J) RorαCre/+;Lhx1loxP/loxP, and (K) RorαCre/Cre;Lhx1loxP/loxP mice subjected to 8 hr phase advance and 8 hr delay. (I) Average (+s.e.m., n = 5–8) activity onset and (K) average (+s.e.m.) number of days to re-entrain to advance or delay in light onset in three genotypes. Color codes in L and M correspond to the labels in I–K.