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

Figure 6. alg-1(anti) mutations affect functions of many microRNAs and exhibit phenotypes more severe than those of alg-1(0).

Figure 6

(A) Plim-6::gfp expression marks ASEL neuronal cell fate in wild type and mutant animals. lsy-6(ot150) mutants lack the Plim-6::gfp expression in the ASEL neurons some of the time. This phenotype is enhanced by the loss of alg-1 and even more so in the presence of either of the two alg-1(anti) mutations. All strains carry lin-31 mutation in order to suppress alg-1(anti) vulval bursting phenotypes by non-heterochronic methods. (B) Combination of alg-1(anti) and alg-2(0) mutations results in embryonic lethality (emb) and early larval lethality (let), with some late larval lethality present in alg-2(0)/+; alg-1(anti)/alg-1(anti) mutant animals. (C, D) Distal tip cell migration phenotypes of wild type and mutant animals. alg-1(anti) mutant animals display defects affecting all three phases of gonad migration. In (C) gonads are marked by a dashed line. (E) alg-1(anti), but not alg-1(0) mutation enhances the embryonic lethality of mir-35–41 mutants. (**p<0.001). All strains carry lin-31(lf) and col-19::gfp in the background. The lin-31 mutation is present in all strains in order to suppress alg-1(anti) vulval bursting phenotypes by non-heterochronic methods. n = number of animals scored.