Neuronal differentiation is highly coordinated through a cascade of gene expression, mediated via interactions between transacting transcription factors and cis-regulatory elements of their target genes. However, the mechanisms of transcriptional regulation that determine neuronal cell-fate are not fully understood. Here, we show that the nuclear transcription factor Y (NF-Y) subunit, NFYA-1, is necessary and sufficient to express the
flp-3 neuropeptide gene in the IL1 neurons of C. elegans.
flp-3 expression is decreased in dorsal and lateral, but not ventral IL1s of
nfya-1 mutants. The expression of another terminally differentiated gene,
eat-4 vesicular glutamate transporter, is abolished, whereas the
unc-8 DEG/ENaC gene and pan-neuronal genes are expressed normally in IL1s of
nfya-1 mutants.
nfya-1 is expressed in and acts in IL1s to regulate
flp-3 and
eat-4 expression. Ectopic expression of NFYA-1 drives the expression of
flp-3 gene in other cell-types. Promoter analysis of IL1-expressed genes results in the identification of several cisregulatory motifs which are necessary for IL1 expression, including a putative CCAAT-box located in the
flp-3 promoter that NFYA-1 directly interacts with. NFYA-1 and NFYA-2, together with NFYB-1 and NFYC-1, exhibit partly or fully redundant roles in the regulation of
flp-3 or
unc-8 expression, respectively. Taken together, our data indicate that the NF-Y complex regulates neuronal subtype-specification via regulating a set of terminal-differentiation genes.