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The Scalloped and Nerfin-1 transcription factors cooperate to maintain neuronal cell fate

ABSTRACT: The Scalloped and Nerfin-1 transcription factors cooperate to maintain neuronal cell fate

PROVIDER: PRJNA494322 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7948880_1.fastq.gz	Fastqsanger.gz
	SRR7948880_2.fastq.gz	Fastqsanger.gz
	SRR7948881_1.fastq.gz	Fastqsanger.gz
	SRR7948881_2.fastq.gz	Fastqsanger.gz
	SRR7948872_1.fastq.gz	Fastqsanger.gz

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The Scalloped and Nerfin-1 transcription factors cooperate to maintain neuronal cell fate

Project description:The ability of cells to stably maintain their fate is governed by specific transcription regulators. Here, we show that the Scalloped (Sd) and Nervous fingers-1 (Nerfin-1) transcription factors physically and functionally interact to maintain medulla neuron fate in the Drosophila melanogaster CNS. Using Targeted DamID we find that Sd and Nerfin-1 occupy a highly overlapping set of target genes, including regulators of neural stem cell and neuron fate, and signalling pathways that regulate CNS development such as Notch and Hippo. Modulation of either Sd or Nerfin-1 activity causes medulla neurons to dedifferentiate to a stem cell-like state and this is mediated at least in part by Notch pathway deregulation. Intriguingly, orthologues of Sd and Nerfin-1 have also been implicated in control of neuronal cell fate decisions in both worms and mammals. Our data indicate that this transcription factor pair exhibits remarkable biochemical and functional conservation across metazoans.

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Project description:Cellular differentiation requires both activation of target cell programs and repression of non-target cell programs. Transcriptional repressors such as RE1-silencing transcription factor (REST) and Hairy/Enhancer of Split (Hes) repress neuronal genes in non-neuronal cells. However, it is unknown whether transcriptional repressors of non-neuronal genes in neuronal precursors are required to specify neuronal fate during development. The Myt1 family of zinc finger transcription factors contributes to fibroblast to neuron reprogramming in vitro by repressing Notch signaling. Here, we show that ztf-11 (Zinc-finger Transcription Factor-11), the sole Caenorhabditis elegans Myt1 homolog, is required for neurogenesis in multiple neuronal lineages, including an in vivo developmental epithelial-to-neuronal transdifferentiation event. ztf-11 is exclusively expressed in all neuronal precursors with remarkable specificity at single cell resolution. Loss of ztf-11 leads to upregulation of non-neuronal genes and reduced neurogenesis. Ectopic expression of ztf-11 in epidermal lineages is sufficient to produce additional neurons. Our genetic and genomic experiments show that ZTF-11 indeed functions as a transcriptional repressor to suppress the activation of non-neuronal genes in neurons; however, it does not function via repression of Notch signaling. Instead, ZTF-11 binds to the MuvBco-repressor complex, which we show is also required for neurogenesis. These results dovetail with ability of Myt1l (Myt1-like) to drive neuronal transdifferentiation in vitro in vertebrate systems. Together, we identified an evolutionarily conserved mechanism to specify neuronal cell fate by repressing non-neuronal genes.

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