Premium
Functional redundancy between Cdc14 phosphatases in zebrafish ciliogenesis
Author(s) -
Clément Aurélie,
SolnicaKrezel Lilianna,
Gould Kathleen L.
Publication year - 2012
Publication title -
developmental dynamics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.634
H-Index - 141
eISSN - 1097-0177
pISSN - 1058-8388
DOI - 10.1002/dvdy.23876
Subject(s) - ciliogenesis , biology , zebrafish , microbiology and biotechnology , cdc25 , cilium , cytokinesis , morpholino , cyclin dependent kinase , centrosome , mitotic exit , cyclin dependent kinase 1 , cell cycle , genetics , cell division , cell , gene , anaphase
Abstract Background: Cyclin‐dependent kinases (Cdks) and their counteracting phosphatases are key regulators of cell cycle progression. In yeasts, the Cdc14 family of phosphatases promotes exit from mitosis and progression through cytokinesis by reversing phosphorylation of Cdk1 substrates. In vertebrates, CDC14 paralogs, CDC14A and CDC14B, have so far been implicated in processes ranging from DNA damage repair, meiosis, centrosome duplication to ciliogenesis. However, the question of whether CDC14 paralogs can functionally compensate for each other has yet to be addressed. Results: Here, using antisense morpholino oligonucleotides to inhibit Cdc14A1 function, we observed that Cdc14A1 depleted zebrafish embryos displayed ventrally curved body and left‐right asymmetry defects, similar to Cdc14B deficient embryos and zebrafish mutants with cilia defects. Accordingly, we found that Cdc14A1, like Cdc14B, plays a role in ciliogenesis in the Kupffer's vesicle (KV) and other ciliated tissues, and can do so independently of its function in cell cycle. Furthermore, we observed reciprocal suppression of KV cilia length defects of Cdc14A1 and Cdc14B deficient embryos by cdc14b and cdc14a1 RNAs, respectively. Conclusions: Together, these studies demonstrate for the first time that Cdc14A and Cdc14B have overlapping functions in the ciliogenesis process during zebrafish development. Developmental Dynamics, 2012. © 2012 Wiley Periodicals, Inc.