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Elife. 2019 Aug 6;8. pii: e46703. doi: 10.7554/eLife.46703.

A Myt1 family transcription factor defines neuronal fate by repressing non-neuronal genes.

Author information

1
Department of Biochemistry, Stanford University, Stanford, United States.
2
Howard Hughes Medical Institute, Stanford University, Stanford, United States.
3
Department of Biology, Stanford University, Stanford, United States.
4
Developmental Biology Program, Sloan-Kettering Institute, New York, United States.
5
Department of Pharmacology, University of California, Davis, Davis, United States.

Abstract

Cellular differentiation requires both activation of target cell transcriptional programs and repression of non-target cell programs. The Myt1 family of zinc finger transcription factors contributes to fibroblast to neuron reprogramming in vitro. 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 from previously differentiated epithelial cells, including a neuron generated by a 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. ZTF-11 functions together with the MuvB corepressor complex to suppress the activation of non-neuronal genes in neurons. These results dovetail with the 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.

KEYWORDS:

C. elegans; MuvB complex; Myt1; ZTF-11; developmental biology; genetics; genomics; neurogenesis; neuronal differentiation; transcriptional repression

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