Treatment of Caenorhabditis elegans with apigenin, 5,7,4'-trihydroxyflavone, induces larval growth inhibition. To understand the molecular basis of apigenin-induced larval growth inhibition, the effects of apigenin on DAF-16 activity were examined. DAF-16 was activated through nuclear translocation and the mRNA level of sod-3, one of the known DAF-16 target genes, was increased upon apigenin treatment. DAF-16 activity was required for the growth inhibition, since the larval growth retardation upon apigenin treatment was suppressed in daf-16 mutants. These results indicate that apigenin acts as a stressor that activates DAF-16, which in turn inhibits larval growth.
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