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

Figure 3. Mutations in alg-1 suppress precocious development of lin-28(lf) (lin-28(n947)) animals.

Figure 3

(A, B) alg-1 mutations suppress the egg-laying defect of lin-28(lf) animals by suppressing the precocious divisions of the vulval precursor cells; (B) Early third larval (eL3) stage animals. Arrowheads indicate vulval cell nuclei. Three vulval precursor cells (P5.p, P6.p, and P7.p) are undivided in the top (N2) and bottom (lin-28(n947); alg-1(ma192)) panels, but in the middle panel (lin-28(n947), P6.p and P7.p have divided twice (one P7.p granddaughter is out of the plane of focus). (C, D) alg-1 mutations suppress the lin-28(lf) precocious expression of the adult cell fate marker col-19::gfp. lL4-late fourth larval stage. (E) alg-1 mutations also increase the seam cell number (#) produced lin-28(lf) mutant animals (***p<0.0001), and (F) suppress precocious alae formation of L4 animals; dotted line represents absence of the alae, solid line underlines the alae structure. All strains col-19::gfp transgene in the background. n = number of animals scored.