Volume 1 Supplement 1
Investigation of a new signalling pathway linking deltaD to ciliogenesis - the role of rabconnectin3
© Tavares et al; licensee BioMed Central Ltd. 2012
Published: 16 November 2012
Recently, using the zebrafish mutant for the deltaD gene (after eight or aei-/-), our group has showed that Notch signaling was involved in the control of cilia length in the cells of the fish laterality organ, the Kupffer’s Vesicle (KV) (Lopes el al. 2010). Further research based on microarray screening allowed the discovery of several genes with differential expression in KV cells from aei-/- mutants compared to WT embryos. One of these genes, rabconnectin3 or rc3 (ENSDARG00000091293) was found to be severely downregulated. Homologs of this gene have recently been associated with Notch signaling in Drosophila and mammalian cells (Yan et al. 2009; Sethi et al. 2010, respectively) through the regulation of the V-ATPase activity. Furthermore, the activity of this pump has also been associated with the ciliogenesis in the KV (Chen et al. 2011). Using a Morpholino against rc3, we caused a decrease in the cilia length of the KV. We propose that the decrease in the cilia size present in the KV of the aei-/- mutants is caused by the deregulation of the transcription of genes such as rc3 and not necessarily by the disruption of the Notch signaling.
- Lopes : Notch signaling regulates left-right asymmetry through ciliary length control. 2010, doi:10.1242/dev.054452Google Scholar
- Yan : The vacuolar proton pump, V-ATPase, is required for notch signaling and endosomal trafficking in Drosophila. 2009, doi:10.1016/j.devcel.2009.07.001Google Scholar
- Sethi : Rabconnectin-3 is a functional regulator of mammalian Notch signaling. 2010, doi:10.1074/jbc.M110.158634Google Scholar
- Chen : A SNX10/V-ATPase pathway regulates ciliogenesis in vitro and in vivo. 2011, doi:10.1038/cr.2011.134Google Scholar
This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.