C2orf62 and TTC17 Are Involved in Actin Organization and Ciliogenesis in Zebrafish and Human
- Authors
- Bontems, F., Fish, R.J., Borlat, I., Lembo, F., Chocu, S., Chalmel, F., Borg, J.P., Pineau, C., Neerman-Arbez, M., Bairoch, A., and Lane, L.
- ID
- ZDB-PUB-140402-20
- Date
- 2014
- Source
- PLoS One 9(1): e86476 (Journal)
- Registered Authors
- Bontems, Franck, Fish, Richard, Lane, Lydie, Neerman-Arbez, Marguerite
- Keywords
- none
- MeSH Terms
-
- Two-Hybrid System Techniques
- Cell Line
- Immunohistochemistry
- Animals
- Actins/physiology*
- Green Fluorescent Proteins
- Gene Expression Profiling
- Sequence Alignment
- Fluorescence Resonance Energy Transfer
- Cilia/genetics
- Cilia/physiology*
- Zebrafish/genetics*
- Humans
- Base Sequence
- DNA Primers/genetics
- Carrier Proteins/genetics
- Carrier Proteins/metabolism*
- Gene Knockdown Techniques
- Real-Time Polymerase Chain Reaction
- Luminescent Proteins
- Computational Biology
- In Situ Hybridization
- Reverse Transcriptase Polymerase Chain Reaction
- PubMed
- 24475127 Full text @ PLoS One
Vertebrate genomes contain around 20,000 protein-encoding genes, of which a large fraction is still not associated with specific functions. A major task in future genomics will thus be to assign physiological roles to all open reading frames revealed by genome sequencing. Here we show that C2orf62, a highly conserved protein with little homology to characterized proteins, is strongly expressed in testis in zebrafish and mammals, and in various types of ciliated cells during zebrafish development. By yeast two hybrid and GST pull-down, C2orf62 was shown to interact with TTC17, another uncharacterized protein. Depletion of either C2orf62 or TTC17 in human ciliated cells interferes with actin polymerization and reduces the number of primary cilia without changing their length. Zebrafish embryos injected with morpholinos against C2orf62 or TTC17, or with mRNA coding for the C2orf62 C-terminal part containing a RII dimerization/docking (R2D2) ? like domain show morphological defects consistent with imperfect ciliogenesis. We provide here the first evidence for a C2orf62-TTC17 axis that would regulate actin polymerization and ciliogenesis.