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The C. elegans COE transcription factor UNC-3 activates lineage-specific apoptosis and affects neurite growth in the RID lineage.

Authors
  • Wang, Jinbo
  • Chitturi, Jyothsna
  • Ge, Qinglan
  • Laskova, Valeriya
  • Wang, Wei
  • Li, Xia
  • Ding, Mei
  • Zhen, Mei
  • Huang, Xun
Type
Published Article
Journal
Development
Publisher
The Company of Biologists
Publication Date
Apr 15, 2015
Volume
142
Issue
8
Pages
1447–1457
Identifiers
DOI: 10.1242/dev.119479
PMID: 25790851
Source
Medline
Keywords
License
Unknown

Abstract

Mechanisms that regulate apoptosis in a temporal and lineage-specific manner remain poorly understood. The COE (Collier/Olf/EBF) transcription factors have been implicated in the development of many cell types, including neurons. Here, we show that the sole Caenorhabditis elegans COE protein, UNC-3, together with a histone acetyltransferase, CBP-1/P300, specifies lineage-specific apoptosis and certain aspects of neurite trajectory. During embryogenesis, the RID progenitor cell gives rise to the RID neuron and RID sister cell; the latter undergoes apoptosis shortly after cell division upon expression of the pro-apoptotic gene egl-1. We observe UNC-3 expression in the RID progenitor, and the absence of UNC-3 results in the failure of the RID lineage to express a Pegl-1::GFP reporter and in the survival of the RID sister cell. Lastly, UNC-3 interacts with CBP-1, and cbp-1 mutants exhibit a similar RID phenotype to unc-3. Thus, in addition to playing a role in neuronal terminal differentiation, UNC-3 is a cell lineage-specific regulator of apoptosis.

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