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Molecular and Cellular Biology, November 2003, p. 8216-8225, Vol. 23, No. 22
0270-7306/03/$08.00+0     DOI: 10.1128/MCB.23.22.8216-8225.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

The Iroquois Homeobox Gene Irx2 Is Not Essential for Normal Development of the Heart and Midbrain-Hindbrain Boundary in Mice

Mélanie Lebel,1,2 Pooja Agarwal,1,2,3 Chi Wa Cheng,1,4 M. Golam Kabir,5,6 Toby Y. Chan,5,6 Vijitha Thanabalasingham,1 Xiaoyun Zhang,1 Dana R. Cohen,1,2 Mansoor Husain,5,6 Shuk Han Cheng,4 Benoit G. Bruneau,1,2,3,5* and Chi-Chung Hui1,2*

Program in Developmental Biology,1 Program in Cardiovascular Research, The Hospital for Sick Children,3 Department of Molecular and Medical Genetics, University of Toronto, Toronto, Ontario M5G 1X8,2 The Heart and Stroke/Richard Lewar Centre for Cardiovascular Research at the University of Toronto,5 Division of Cellular and Molecular Biology, Toronto General Hospital Research Institute, Toronto General Hospital, and Department of Medicine, University of Toronto, Toronto, Ontario M5G 2C4, Canada,6 Department of Biology and Chemistry, City University of Hong Kong, Kowloon, Hong Kong, China4

Received 11 April 2003/ Returned for modification 12 June 2003/ Accepted 14 August 2003

The Iroquois homeobox (Irx) genes have been implicated in the specification and patterning of several organs in Drosophila and several vertebrate species. Misexpression studies of chick, Xenopus, and zebra fish embryos have demonstrated that Irx genes are involved in the specification of the midbrain-hindbrain boundary. All six murine Irx genes are expressed in the developing heart, suggesting that they might possess distinct functions during heart development, and a role for Irx4 in normal heart development has been recently demonstrated by gene-targeting experiments. Here we describe the generation and phenotypic analysis of an Irx2-deficient mouse strain. By targeted insertion of a lacZ reporter gene into the Irx2 locus, we show that lacZ expression reproduces most of the endogenous Irx2 expression pattern. Despite the dynamic expression of Irx2 in the developing heart, nervous system, and other organs, Irx2-deficient mice are viable, are fertile, and appear to be normal. Although chick Irx2 has been implicated in the development of the midbrain-hindbrain region, we show that Irx2-deficient mice develop a normal midbrain-hindbrain boundary. Furthermore, Irx2-deficient mice have normal cardiac morphology and function. Functional compensation by other Irx genes might account for the absence of a phenotype in Irx2-deficient mice. Further studies of mutant mice of other Irx genes as well as compound mutant mice will be necessary to uncover the functional roles of these evolutionarily conserved transcriptional regulators in development and disease.

* Corresponding authors. Mailing address: Program in Developmental Biology, The Hospital for Sick Children, 555 University Ave., Toronto, Ontario M5G 1X8, Canada. Phone: (416) 813-5681. Fax: (416) 597-9497. E-mail for Chi-Chung Hui: cchui{at}sickkids.ca. E-mail for Benoit G. Bruneau: bbruneau{at}sickkids.ca. Mailing address for Hui Chi-Chung: Program in Developmental Biology, The Hospital for Sick Children, 555 University Ave., Toronto, Ontario M5G 1X8, Canada. Phone: (416) 813-5681. Fax: (416) 597-9497. E-mail for Chi-Chung Hui: cchui{at}sickkids.ca.

Molecular and Cellular Biology, November 2003, p. 8216-8225, Vol. 23, No. 22
0022-538X/03/$08.00+0     DOI: 10.1128/MCB.23.22.8216-8225.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.



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