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RESEARCH ARTICLE Open Access The Caenorhabditis elegans CDT-2 ubiquitin ligase
 

Summary: RESEARCH ARTICLE Open Access
The Caenorhabditis elegans CDT-2 ubiquitin ligase
is required for attenuation of EGFR signalling in
vulva precursor cells
Gino B Poulin1*
, Julie Ahringer2
Abstract
Background: Attenuation of the EGFR (Epidermal Growth Factor Receptor) signalling cascade is crucial to control
cell fate during development. A candidate-based RNAi approach in C. elegans identified CDT-2 as an attenuator of
LET-23 (EGFR) signalling. Human CDT2 is a component of the conserved CDT2/CUL4/DDB1 ubiquitin ligase
complex that plays a critical role in DNA replication and G2/M checkpoint. Within this complex, CDT2 is responsible
for substrate recognition. This ubiquitin ligase complex has been shown in various organisms, including C. elegans,
to target the replication-licensing factor CDT1, and the CDK inhibitor p21. However, no previous link to EGFR
signalling has been identified.
Results: We have characterised CDT-2's role during vulva development and found that it is a novel attenuator of
LET-23 signalling. CDT-2 acts redundantly with negative modulators of LET-23 signalling and CDT-2 or CUL-4
downregulation causes persistent expression of the egl-17::cfp transgene, a marker of LET-23 signalling during vulva
development. In addition, we show that CDT-2 physically interacts with SEM-5 (GRB2), a known negative modulator
of LET-23 signalling that directly binds LET-23, and provide genetic evidence consistent with CDT-2 functioning at
or downstream of LET-23. Interestingly, both SEM-5 and CDT-2 were identified independently in a screen for genes

  

Source: Ahringe, Julie - Wellcome Trust/Cancer Research UK Gurdon Institute, University of Cambridge

 

Collections: Biology and Medicine