Table of Contents Author Guidelines Submit a Manuscript
BioMed Research International
Volume 2014 (2014), Article ID 309385, 11 pages
http://dx.doi.org/10.1155/2014/309385
Research Article

Characterization of Zebrafish Pax1b and Pax9 in Fin Bud Development

1Faculty of Basic Medical Sciences, Chongqing Medical University, Medical College Road 1, Chongqing 400016, China
2Emergency Department, The First Affiliated Hospital of Chongqing Medical University, Youyi Road 1, Chongqing 400042, China
3School of Life Sciences, Xiamen University, South Xiang’an Road, Xiamen 361102, China
4Department of Nephrology, The First Affiliated Hospital of Chongqing Medical University, Youyi Road 1, Chongqing 400042, China
5Department of Cardiology, The First Affiliated Hospital of Chongqing Medical University, Youyi Road 1, Chongqing 400042, China

Received 3 April 2014; Revised 31 May 2014; Accepted 1 July 2014; Published 13 August 2014

Academic Editor: Bryan Crawford

Copyright © 2014 Xuemei Chen et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Both Pax1 and Pax9 belong to the important paired box gene family (PAX), which mainly participates in animal development and sclerotome differentiation. To date, the precise molecular mechanism and related signaling pathway of Pax1 remain unclear. In our study, microinjection of morpholino- (MO-) modified antisense oligonucleotides against pax1b induced pectoral fin bud defects. Furthermore, we demonstrate that the phenotypes caused by the knockdown of Pax1b in zebrafish could not be phenocopied by pax9 MO and could not be rescued by either Pax1a or Pax9 overexpression. We further find that Pax1b affects the expression of col2a1, Uncx4.1, Noggin3, and aggrecan, confirming the role of Pax1b in chondrocyte differentiation and bone maturation. Moreover, we identify an interaction between PAX1 and FOXO1 and find that the interaction was enhanced under hypoxia stress. Together, this evidence for cell death caused by pax1b knockdown provides new insight into the role of the Pax protein family in cell fate determination and tissue specification.