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. 2021 Oct 12;220(2):iyab174. doi: 10.1093/genetics/iyab174

Figure 1.

Figure 1

AtTIR1(WT) induces a lin-28 loss-of-function phenotype in the absence of exogenously added auxin ligand. (A) The lateral seam cells of wild-type C. elegans larva exhibit a stereotyped cell division program that generates additional seam cell in the L2 stage. Mutations in the heterochronic gene lin-28 result in an altered seam cell division pattern due to the skipping of L2 stage-specific developmental programs. In addition, the lateral seam cells lin-28(0) mutants precociously exit the cell cycle and inappropriately deposit alae, adult-specific cuticle structures, during the L3–L4 molt. (B) In contrast to the normal skin and vulval developmental programs of wild-type animals and animals that harbor an AID-tagged lin-28 allele, lin-28(0) mutants exhibit precocious alae at the L4 stage and a protruding vulval phenotype (pvl). (C) Combining the AID-tagged lin-28 allele with a ubiquitously expressed AtTIR1(WT) allele results in strong heterochronic phenotypes in the absence of additional auxin. Dashed yellow lines indicate the absence of adult stage-specific alae structures whereas a solid line demarcates the presence of adult stage-specific alae structures (see Table  1 for details).