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The CCAAT-box transcription factor, NF-Y complex, mediates neuronal specification of the IL1 neurons in C. elegans
Woojung Heo1 (Graduate student), Hyeonjeong Hwang1 (Graduate student), Jimin Kim1 (Graduate student), SeungHee Oh1 (Graduate student), Youngseok Yu2 (Graduate student), Jae-Hyung Lee1 (Professor), Kyuhyung Kim 1,* (Professor)
1Brain Sciences, DGIST,
2Life and Nanopharmaceutical Sciences and 3Oral Microbiology, Kyung Hee University
Neuronal differentiation is highly coordinated through a cascade of gene expression, mediated via interactions between trans-acting 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 cis-regulatory 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.
Abstract, Accepted Manuscript(in press) [Submitted on September 16, 2022, Accepted on October 27, 2022]
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