Figure 1.
Independent control over PER and CRY protein stabilities by CK1ε
Tau
and Fbxl3Afh
alleles.
a
, Western blots for CRY1 in single representative SCN slices carrying either wild-type, CK1ε
Tau
, or Fbxl3Afh
alleles, treated with CHX at CT12 and harvested immediately or after 12 h. Right, Blots from CRY2 and CRY1 null mice confirm specificity of antiserum; bottom panels, actin loading controls.
b
, Group data (mean ± SEM, n = 3–4 SCNs per observation) reveal significant (ANOVA, p < 0.01) reduction in rate of CRY degradation in Afh mutant, with (diamond) and without (triangle) Tau mutation compared to wild type (circle).
c
, Group data (mean ± SEM, n = 6–8 SCNs per genotype) for PER2 half-life across genotypes. *p < 0.05 significant versus wild-type control, +++
p < 0.001 versus Afh mutant.