The C. elegans Tailless/TLX transcription factor nhr-67 controls neuronal identity and left/right asymmetric fate diversification -- Sarin et al. 136 (17): 2933 Data Supplement - DEV040204 Supplementary Material -- Development

DEV040204 Supplementary Material

Files in this Data Supplement:

Supplemental Table S1 -
Supplemental Figure S1 -
Fig. S1. Loss of ASE fate markers not due to apoptotic cell death. Animals were scored as adults, using the otIs114 transgene.
Supplemental Figure S2 -
Fig. S2. Quantification of nhr-67 effect on che-1 expression. Animals were scored as embryos at given morphological stages, using the otIs188 transgene.
Supplemental Figure S3 -
Fig. S3. The excretory canal cells display a cystic phenotype in nhr-67 mutants. The lumen of the canal cell is visualized with a pes-6::gfp reporter gene. Defects can be observed in 5% of arrested ok631 L1 mutant animals. Similar defects were also observed with another nhr-67 allele, ot407.