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. 2015 Sep 10;4:e05842. doi: 10.7554/eLife.05842

Figure 8. Exposure to 1 nM LY411575 rescues the delay in clock gene oscillations caused by Roscovitine, DRB and XAV939.

Bissected chick or mouse caudal explant pairs treated ‘−’ or ‘+’ inhibitor and then analysed by insitu hybridisation for Lfng mRNA expression: (AC) Treatment of chick PSM explants in the presence (+) or absence (−) of 5 nM LY411575 (A), 1 nM LY411575 (B), 0.1 nM LY411575 (C) for 3 hr reveals that 5 nM LY411575 severely downregulates cLfng expression whereas 1 nM and 0.1 nM do not appear to change levels or domain of cLfng expression. (DF): Treatment of chick PSM explants in the presence (+) or absence (−) of Roscovitine (D), DRB (E) or XAV939 (F) for 3 hr reveals that ‘+’ explants have lagging expression of cLfng, with one less somite formed than the ‘−’ explants. (GI): Treatment of chick PSM explants in the presence (+) or absence (−) of 1 nM LY411575 together with Roscovitine (G), DRB (H) or XAV939 (I) for 3 hr reveals that 1 nM LY411575 rescues the delay in clock gene oscillations caused by these three inhibitors such that the cLfng expression domains in the ‘−’ and ‘+’ explants are very similar. The red arrowheads identify the somites formed during the in vitro culture period of the assay. (P) = previous cycle.

DOI: http://dx.doi.org/10.7554/eLife.05842.017

Figure 8.

Figure 8—figure supplement 1. 0.1 nM LY411575 does not rescue the delay in oscillation caused by Roscovitine.

Figure 8—figure supplement 1.

Bissected chick caudal explant pair treated ‘−’ or ‘+’ 10μM roscovitine and 0.1 nM LY411575 and then analysed by in situ hybridisation for the Notch target gene cLfng reveals cLfng mRNA expression is delayed in the treated side as compared to the control after 3 hr treatment. Black arrows indicate somites.