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. 2014 Apr 24;10(4):e1004286. doi: 10.1371/journal.pgen.1004286

Figure 11. Model representing a proposed mode of action of antimorphic mutant ALG-1.

Figure 11

(A) In wild type animals, ALG-1 and ALG-2 associate with microRNA precursors (Loading), act in conjunction with Dicer to facilitate cleavage of the precursor to yield mature microRNA (Dicing), and through a series of miRISC maturation steps, associate with effector partners including AIN-1/GW182, and repress mRNA targets (Maturation/Function). According to the model, ALG-1 and ALG-2 are partially redundant, and function asymmetrically; ALG-1 carries a majority share of microRNA function. (B) In the absence of ALG-1, ALG-2 is able to partially cover for reduced overall ALG activity, and so alg-1(0) animals exhibit weak microRNA loss-of-function phenotypes, and accumulate abnormal levels of microRNA precursors. (C) In alg-1(anti) animals, microRNA activity is globally poisoned by the ALG-1(anti) protein. This is because ALG-1(anti) protein is competent for Loading and Dicing, but is blocked in one or more steps of miRISC maturation wherein ALG-1 would normally transition from Dicer associated microRNA processing to AIN-1/GW182 associated target repression. This hypothetical miRISC maturation defect results in sequestration of miRISC components (including microRNAs) in inactive complexes. Jagged lines attached to ribosomes (brown ovals) represent un-repressed protein synthesis from target mRNA.