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Molecular and Cellular Biology, August 2004, p. 7102-7112, Vol. 24, No. 16
0270-7306/04/$08.00+0 DOI: 10.1128/MCB.24.16.7102-7112.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.
T. Ott,2,
C. Lance-Jones,1 G. Schuetz,3 A. Schwaeger-Nickolenko,3 and A. P. Monaghan1*
Department of Neurobiology, School of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania 15261,1 Department of Molecular Genetics, Institute for Genetics, 53117 Bonn,2 Division of Molecular Biology of the Cell I, German Cancer Research Center, D-69120 Heidelberg, Germany3
Received 7 July 2003/ Returned for modification 22 August 2003/ Accepted 14 May 2004
Members of the Spalt gene family encode putative transcription factors characterized by seven to nine C2H2 zinc finger motifs. Four genes have been identified in miceSpalt1 to Spalt4 (Sall1 to Sall4). Spalt homologues are widely expressed in neural and mesodermal tissues during early embryogenesis. Sall3 is normally expressed in mice from embryonic day 7 (E7) in the neural ectoderm and primitive streak and subsequently in the brain, peripheral nerves, spinal cord, limb buds, palate, heart, and otic vesicles. We have generated a targeted disruption of Sall3 in mice. Homozygous mutant animals die on the first postnatal day and fail to feed. Examination of the oral structures of these animals revealed that abnormalities were present in the palate and epiglottis from E16.5. In E10.5 embryos, deficiencies in cranial nerves that normally innervate oral structures, particularly the glossopharyngeal nerve (IX), were observed. These studies indicate that Sall3 is required for the development of nerves that are derived from the hindbrain and for the formation of adjacent branchial arch derivatives.
M.P. and T.O. contributed equally to this work.
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