Catalysts for Solar Fuel Production

expression of a dcr-1 transgene that lacks a cleavage site for CED-3 rescued the devel-opmental (vulva) defect, but not the apop-totic phenotype. Conversely, transgenic expression of the truncated form of Dcr-1 in dcr-1 mutants rescued apoptosis but not the vulvar phenotype. This highly unexpected role for Dcr-1 in early apoptotic DNA degradation has numer-ous important implications. Caspase-medi-ated activation of DNA degradation now appears conserved from nematodes to mam-mals. Full-length Dcr-1 (and/or Dcr-1 in complex with a dsRBP) maintains an inac-tive DNase in a manner similar to the DFF40-DFF45 complex in mammals. Cleavage of Dcr-1 by CED-3 activates a functional DNase that generates 3 ′ hydroxyl DNA breaks, which are subsequently resolved by progres-sive DNases. Conservation of this enzymatic switch may mean that Dicer also serves as an apoptotic DNase in higher organisms. The DNase activity of Dicer may also gov-ern other aspects of chromosome dynamics. Thus, it may be prudent to consider RNAi-independent mechanisms underlying the phe-notypes of dicer mutants. Perhaps most excit-ing will be determining the extent to which regulators of nucleic acid function exhibit substrate crossover, and the mechanisms through which this switching may occur