Selected article for: "cell apoptosis and egg production"
Author: Yang, H-C; Chen, T-L; Wu, Y-H; Cheng, K-P; Lin, Y-H; Cheng, M-L; Ho, H-Y; Lo, S J; Chiu, D T-Y
Title: Glucose 6-phosphate dehydrogenase deficiency enhances germ cell apoptosis and causes defective embryogenesis in Caenorhabditis elegans
  • Document date: 2013_5_2
    • ID: j3ku7i2c_14
    Snippet: All in all, we have reported a reproducible method to generate G6PD-deficient C. elegans by RNAi technique. This G6PD-knockdown animal model allows us to delineate the chronic effects of G6PD-deficiency at the multicellular organism level. The parental G6PD-knockdown C. elegans is viable and shows no major growth defect. However, G6PD-knockdown C. elegans displays enhanced germ cell apoptosis and reduced egg production as well as a severe defect .....
    Document: All in all, we have reported a reproducible method to generate G6PD-deficient C. elegans by RNAi technique. This G6PD-knockdown animal model allows us to delineate the chronic effects of G6PD-deficiency at the multicellular organism level. The parental G6PD-knockdown C. elegans is viable and shows no major growth defect. However, G6PD-knockdown C. elegans displays enhanced germ cell apoptosis and reduced egg production as well as a severe defect in hatching. Mechanistic studies suggest that decreased egg production in G6PD-knockdown C. elegans could be attributed in part to increased oxidative stress and oxidative damage. In contrast to its toxic effect in egg production, ROS may play an important role as signal molecules to mediate MAPK pathway that in turn can affect hatching in C. elegans.

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