The Hox gene lin-39 may play a role in initiating the 1° cell fate during vulval development in C. elegans. This cell fate specification process is triggered by a Ras/MAPK signal transduction cascade, wherein the transcription factors LIN-1 and LIN-31 are activated in order to upregulate expression of lin-39. However, the mechanistic details behind LIN-1 and LIN-31 regulation are not fully understood. Prior to activation, LIN-1 is SUMOlyated and serves as a transcriptional repressor, while the post-translational and transcriptional states of LIN-31 are unknown. Phosphorylation appears to convert LIN-1 and LIN-31 into transcriptional activators. Preliminary evidence from an electrophoretic mobility shift assay (EMSA) may indicate that SUMOlyation represses LIN-31 DNA-binding activity. Moreover, structural analysis of LIN-31 may suggest that SUMO serves as a linker that mediates the formation of a heterodimer between LIN-1 and LIN-31. Altogether, these findings may imply that LIN-1 and LIN-31 are concurrently regulated in similar manners, such that SUMOlyation acts as an OFF switch and phosphorylation acts as an ON switch for transcriptional activity. A variety of molecular techniques will be used to elucidate the regulatory dynamics of LIN-1 and LIN-31. EMSA and ChIP-seq will be used to determine the precise binding site of LIN-1 and LIN-31 on the lin-39 promoter as well as to test the heterodimerization between LIN-1 and LIN-31. Further experiments with the CRISPR/Cas9 genome editing system will query whether particular structural elements on each transcription factor are necessary for proper regulation of vulval development.