Fig. 6: Knockdown of chk-1 and pkc-1 shows complete and partial rescue of dysfunctions in agl-1 mutants.

A Knockdown of chk-1 in S1444R C. elegans mutant shows significant and specific rescue in glycogen buildup phenotype (n ≈ 30); **p = 0.0071. B Knockdown of pkc-1 in S1444R C. elegans mutant shows significant and specific rescue in glycogen buildup phenotype (n ≈ 30); ****p < 0.0001. C S1444R and Δagl-1 mutants show significantly increased RNA expression of the chk-1 gene (N = 3); **p < 0.01. D W1044X, S1444R, Δagl-1 mutants and wild-type have a similar expression of the pkc-1 gene. E chk-1 downregulation rescues the progressive paralysis on solid media in S1444R mutant (n ≈ 360); ****p < 0.0001. F pkc-1 knockdown does not rescue the progressive paralysis phenotype in S1444R mutants. G Pharmacological inhibition of CHK1 rescues glycogen buildup (n ≈ 30) and H paralysis phenotypes (n ≈ 360); p = 0.0433, ****p < 0.0001. I Knockdown of aak-2 in S1444R mutants shows no change in glycogen buildup phenotype (n ≈ 30) and (J) no changes in chk-1 expression (N = 3). One-way ANOVAs with Welch’s correction applied when variances were unequal were performed for A (DF = 3, F(3, 80) = 1.513), B (DF = 3, F(3, 75) = 0.7404), C (DF = 4, F(3.000, 6.050) = 32.49) and D (DF = 4, F(3.000, 4.360) = 5.601). Log-rank (Mantel–Cox) tests were used for E (DF = 1), F (DF = 1), and H (DF = 4). Unpaired t-tests with Welch correction were performed for G (t = 2.347, DF = 65.20), I (t = 1.480, DF = 43.69), J (t = 1.059, DF = 3.324). Data are presented as mean ± SEM.