Format

Send to

Choose Destination
Dev Biol. 2017 Sep 1;429(1):240-248. doi: 10.1016/j.ydbio.2017.06.022. Epub 2017 Jun 30.

Distinct cis elements in the 3' UTR of the C. elegans cebp-1 mRNA mediate its regulation in neuronal development.

Author information

1
Section of Neurobiology, Division of Biological Sciences, University of California San Diego, La Jolla, CA 92093, USA.
2
Howard Hughes Medical Institute, USA.
3
Section of Neurobiology, Division of Biological Sciences, University of California San Diego, La Jolla, CA 92093, USA; Howard Hughes Medical Institute, USA. Electronic address: yijin@ucsd.edu.

Abstract

The 3' untranslated regions (3' UTRs) of mRNAs mediate post-transcriptional regulation of genes in many biological processes. Cis elements in 3' UTRs can interact with RNA-binding factors in sequence-specific or structure-dependent manners, enabling regulation of mRNA stability, translation, and localization. Caenorhabditis elegans CEBP-1 is a conserved transcription factor of the C/EBP family, and functions in diverse contexts, from neuronal development and axon regeneration to organismal growth. Previous studies revealed that the levels of cebp-1 mRNA in neurons depend on its 3' UTR and are also negatively regulated by the E3 ubiquitin ligase RPM-1. Here, by systematically dissecting cebp-1's 3' UTR, we test the roles of specific cis elements in cebp-1 expression and function in neurons. We present evidence for a putative stem-loop in the cebp-1 3' UTR that contributes to basal expression levels of mRNA and to negative regulation by rpm-1. Mutant animals lacking the endogenous cebp-1 3' UTR showed a noticeable increased expression of cebp-1 mRNA and enhanced the neuronal developmental phenotypes of rpm-1 mutants. Our data reveal multiple cis elements within cebp-1's 3' UTR that help to optimize CEBP-1 expression levels in neuronal development.

KEYWORDS:

Axon regeneration; Mechanosensory neurons; Stem-loop; Translation regulation; mRNA secondary structure; mRNA stability; rpm-1

PMID:
28673818
PMCID:
PMC5828015
DOI:
10.1016/j.ydbio.2017.06.022
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Elsevier Science Icon for PubMed Central
Loading ...
Support Center