Sensory organ remodeling in Caenorhabditis elegans requires the zinc-finger protein ZTF-16.

Abstract:

:Neurons and glia display remarkable morphological plasticity, and remodeling of glia may facilitate neuronal shape changes. The molecular basis and control of glial shape changes is not well understood. In response to environmental stress, the nematode Caenorhabditis elegans enters an alternative developmental state, called dauer, in which glia and neurons of the amphid sensory organ remodel. Here, we describe a genetic screen aimed at identifying genes required for amphid glia remodeling. We previously demonstrated that remodeling requires the Otx-type transcription factor TTX-1 and its direct target, the receptor tyrosine kinase gene ver-1. We now find that the hunchback/Ikaros-like C2H2 zinc-finger factor ztf-16 is also required. We show that ztf-16 mutants exhibit pronounced remodeling defects, which are explained, at least in part, by defects in the expression of ver-1. Expression and cell-specific rescue studies suggest that ztf-16, like ttx-1, functions within glia; however, promoter deletion studies show that ztf-16 acts through a site on the ver-1 promoter that is independent of ttx-1. Our studies identify an important component of glia remodeling and suggest that transcriptional changes may underlie glial morphological plasticity in the sensory organs of C. elegans.

journal_name

Genetics

journal_title

Genetics

authors

Procko C,Lu Y,Shaham S

doi

10.1534/genetics.111.137786

subject

Has Abstract

pub_date

2012-04-01 00:00:00

pages

1405-15

issue

4

eissn

0016-6731

issn

1943-2631

pii

genetics.111.137786

journal_volume

190

pub_type

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