Characterization of the C. elegans erlin homologue |
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| Authors: | Maja B Hoegg Stephen M Robbins and James D McGhee |
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| Institution: | (1) Department of Biochemistry & Molecular Biology, University of Calgary, 3330 Hospital Drive NW, Calgary, Alberta, T2N 4N1, Canada;(2) Department of Oncology, University of Calgary, 3330 Hospital Drive NW, Calgary, Alberta, T2N 4N1, Canada;(3) Southern Alberta Cancer Research Institute, University of Calgary, 3330 Hospital Drive NW, Calgary, Alberta, T2N 4N1, Canada;(4) Department of Medical Genetics, University of Calgary, 3330 Hospital Drive NW, Calgary, Alberta, T2N 4N1, Canada;(5) Alberta Children’s Hospital Research Institute, University of Calgary, 3330 Hospital Drive NW, Calgary, Alberta, T2N 4N1, Canada |
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| Abstract: | Background Erlins are highly conserved proteins associated with lipid rafts within the endoplasmic reticulum (ER). Biochemical studies
in mammalian cell lines have shown that erlins are required for ER associated protein degradation (ERAD) of activated inositol-1,4,5-trisphosphate
receptors (IP3Rs), implying that erlin proteins might negatively regulate IP3R signalling. In humans, loss of erlin function
appears to cause progressive intellectual disability, motor dysfunction and joint contractures. However, it is unknown if
defects in IP3R ERAD are the underlying cause of this disease phenotype, whether ERAD of activated IP3Rs is the only function
of erlin proteins, and what role ERAD plays in regulating IP3R-dependent processes in the context of an intact animal or embryo.
In this study, we characterize the erlin homologue of the nematode Caenorhabditis elegans and examine erlin function in vivo. We specifically set out to test whether C. elegans erlin modulates IP3R-dependent processes, such as egg laying, embryonic development and defecation rates. We also explore
the possibility that erlin might play a more general role in the ERAD pathway of C. elegans. |
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