Fig. 2: Behavioral characterization of C. elegans GSDIII disease models shows significantly impaired development and aging phenotypes. | Communications Biology

Fig. 2: Behavioral characterization of C. elegans GSDIII disease models shows significantly impaired development and aging phenotypes.

From: CHK1 inhibition rescues abnormal glycogen buildup in a Caenorhabditis elegans model for glycogen storage disease III

Fig. 2: Behavioral characterization of C. elegans GSDIII disease models shows significantly impaired development and aging phenotypes.

A agl-1 mutants show significantly decreased survival compared to wild-type (n ≈ 360). B All agl-1 mutants have a significantly reduced number of offspring compared to wild-type animals (n ≈ 30). C agl-1 mutants show significant developmental delay compared to wild-type (n ≈ 300). D S1444R C. elegans mutant displays significantly impaired swimming motility behavior at day 1 of adulthood (n ≈ 360). E S1444R mutants show greater motility defects leading to paralysis on solid media compared to wild-type, W1044X, and deletion mutants (n ≈ 360). Log-rank (Mantel–Cox) tests were used for A (DF = 3) and E (DF = 1). A one-way ANOVA was performed for B (DF = 3, F(3,107) = 0.03231). Two-way ANOVAs were performed for C (DF = 4, F(4, 10) = 137.1) and D (DF = 3, F(3,32) = 39.31). Data are presented as mean ± SEM.

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