Figure 6.

Asymmetric lsy-6 Competence Is Maintained in a Symmetric Trans-acting Factor Environment

(A) Schematics of the developmental lineage and representative images of embryos of the indicated genotypes. The ASE neurons are marked by che-1^prom::mCherry. (Left) 41/41 wild-type embryos express the lsy-6::yfp^fosmid reporter in ASEL. Light-red highlight of the lineage indicates potential downstream asymmetries triggered by TBX-37/38. (Middle) Deletion of tbx-37/38 resulted in 22/22 embryos without lsy-6::yfp^fosmid expression. (Right) Heterologous, asymmetric priming using the lsy-6::gfp::Δtbs::5xUAS + tbx-37^prom::gal4::vp64 system (Figure 5B) was sufficient to activate lsy-6::yfp expression in only one ASE neuron in tbx-37/38(0) animals. Three independent transgenic lines were scored, numbers of embryos are shown. All scale bars represent 10 μm.

(B) The ubiquitous TF lsy-2 is necessary for robust lsy-6::yfp^fosmid expression in ASEL (Table S3). Progeny of lsy-2 heterozygous mothers were scored as larvae for YFP expression and compared with wild type. 25% of larvae are expected to be homozygous for lsy-2, setting the maximum possible effect. Animals scored as “dim” had a barely visible signal. n ≥ 113 per genotype.

(C) Deletion of an E-box in the lsy-6 locus causes a delay in onset of lsy-6::yfp expression. Expression was scored in embryos from comma to 2-fold stage (early embryos, e.e.) or at the 3-fold stage (late embryos, l.e.). Three independent extrachromosomal lines show a delay in onset of YFP expression, n ≥ 22 per condition (Table S3).