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. 2010 Jul 1;107(29):12907–12912. doi: 10.1073/pnas.1000979107

Fig. 7.

Fig. 7.

Shh and RA signaling pathways interplay in the PSM to ensure timely somite formation. (A and B) Retinoic acid mediates the recovery of timely somite formation in absence of notochord. (A) Explants with (No+) or without (No−) notochord were cultured for 9 h with DMSO (control explant) or with 15 μM of retinoic acid (RA) (experimental explant). Black arrowheads indicate somites formed before culture; white arrowheads indicate somites formed during incubation period (New so). (B) Graphic representation of mean number of somites formed by explants with notochord (No+), without notochord (No−) or without notochord but with RA (No−/RA+). **P < 0.05 vs. No+ or No−/RA. ns, Not statistically significant. Data are mean ± SD. (C) Proposed model for molecular events underlying temporal control of somite formation in the presence (No+) or absence (No−) of notochord over time. In the presence of notochord-derived Shh, gli2/3 expression in the PSM is repressed, and timely molecular clock oscillations and somite formation occur. When Shh signaling is disrupted, gli2/3 are overexpressed, and there is a delay in both the clock period and PSM morphological segmentation. The normal rate of these events is reestablished over time due to an up-regulation of RA that counteracts Gli activity (detailed in text).