Ben Xu and Arun Hariharan contributed equally to this work.
The role of Pax2 in mouse prostate development†
Version of Record online: 18 MAY 2011
Copyright © 2011 Wiley Periodicals, Inc.
Volume 72, Issue 2, pages 217–224, 1 February 2012
How to Cite
Xu, B., Hariharan, A., Rakshit, S., Dressler, G. R. and Wellik, D. M. (2012), The role of Pax2 in mouse prostate development. Prostate, 72: 217–224. doi: 10.1002/pros.21424
- Issue online: 22 DEC 2011
- Version of Record online: 18 MAY 2011
- Manuscript Accepted: 28 APR 2011
- Manuscript Received: 11 MAR 2011
- NIH. Grant Number: DK077045
- prostate development;
- prostate lobe-specific markers
Loss-of-function of Pax2 results in severe defects of the male reproductive system, and Pax2 expression is detected in mouse prostate lobes and human prostatic cancers. However, the role for Pax2 in prostate development remains poorly understood.
The expression of Pax2 was examined by in situ hybridization at various developmental stages. Urogenital sinuses were dissected out at E18.5 from mouse Pax2 mutants and controls, cultured in vitro or grafted under the renal capsule of CD1 nude mice. The expression of prostate developmental regulatory factors was analyzed by semi-quantitative real-time PCR or immuohistochemistry.
Pax2 is expressed in the epithelial cells of prostate buds. Loss-of-function of Pax2 does not affect the initiation of prostatic buds, but in vitro culture assays show that the prostates of Pax2 mutants are hypomorphic and branching is severely disrupted compared to controls. RT-PCR data from Pax2 mutant prostates demonstrate increased expression levels of dorsolateral prostate marker MSMB and ventral prostate marker SBP and dramatically reduced expression levels of anterior prostate marker TGM4.
Pax2 is essential for mouse prostate development and regulates prostatic ductal growth, branching, and lobe-specific identity. These findings are important for understanding the molecular regulatory mechanisms in prostate development. Prostate 72:217–224, 2012. © 2011 Wiley Periodicals, Inc.