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Molecular and Cellular Biology, January 2003, p. 62-69, Vol. 23, No. 1
0270-7306/03/$08.00+0     DOI: 10.1128/MCB.23.1.62-69.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

Zinc Finger Protein Sall2 Is Not Essential for Embryonic and Kidney Development

Akira Sato,1,2 Yuko Matsumoto,1 Urara Koide,1,2 Yuki Kataoka,3 Nobuaki Yoshida,3 Takashi Yokota,1 Makoto Asashima,2 and Ryuichi Nishinakamura1*

Division of Stem Cell Regulation,1 Laboratory of Gene Expression and Regulation, The Institute of Medical Science, The University of Tokyo, Tokyo 108-8639,3 Department of Life Sciences, The University of Tokyo, Tokyo 153-8902, Japan2

Received 5 June 2002/ Returned for modification 19 July 2002/ Accepted 1 October 2002

SALL/Sall is a mammalian homolog of the Drosophila region-specific homeotic gene spalt (sal), and heterozygous mutations in SALL1 in humans lead to Townes-Brocks syndrome. We earlier reported that mice deficient in Sall1 die in the perinatal period and that kidney agenesis or severe dysgenesis are present. We have now generated mice lacking Sall2, another Sall family gene. Although Sall2 is expressed mostly in an overlapping fashion versus that of Sall1, Sall2-deficient mice show no apparent abnormal phenotypes. Morphology and gene expression patterns of the mutant kidney were not affected. Mice lacking both Sall1 and Sall2 show kidney phenotypes comparable to those of Sall1 knockout, thereby demonstrating the dispensable roles of Sall2 in embryonic and kidney development.

* Corresponding author. Mailing address: Division of Stem Cell Regulation, The Institute of Medical Science, The University of Tokyo, Tokyo 108-8639, Japan. Phone: 81-3-5449-5736. Fax: 81-3-5449-5450. E-mail: ryuichi{at}ims.u-tokyo.ac.jp.

Molecular and Cellular Biology, January 2003, p. 62-69, Vol. 23, No. 1
0022-538X/03/$08.00+0     DOI: 10.1128/MCB.23.1.62-69.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.



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