“…However, we discovered that PRC2.1 did not directly bind to neuronal genes in these cells and that, instead, it targeted transcription factors involved in sensory neuron development, synaptic function, and axon targeting. Specifically, on a high sugar diet Pcl binding was increased at the cad , GATAe , nub/pdm , Ptx1 loci and decreased at the Scro locus, with corresponding changes in the mRNA levels of these genes ( Interestingly, several of the transcription factors we identified -Ptx1 , Scro , and nub/pdm -have been shown to control the proper branching, synaptic connectivity, and function of sensory neurons (Corty et al, 2016;Iyer et al, 2013;Neumann and Cohen, 1998;Parrish et al, 2006Parrish et al, , 2007Vorbrüggen et al, 1997;Zaffran et al, 2000) , while others ( cad , nub/pdm ) play a role in neuroblast development (Doe, 2017;Kohwi and Doe, 2013) ; PRC2 also functions as a competence factor in neural proliferation, differentiation and sensory neurons (Bahrampour et al, 2019;Doe, 2017;Parrish et al, 2007) . Importantly, we found that the 4 activators that are repressed by Pcl in the high sugar condition are enriched in the Gr5a+ cells on a control diet, while Scro is depleted.…”