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Molecular and Cellular Biology, March 2001, p. 1484-1490, Vol. 21, No. 5
0270-7306/01/$04.00+0   DOI: 10.1128/MCB.21.5.1484-1490.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Dach1 Mutant Mice Bear No Gross Abnormalities in Eye, Limb, and Brain Development and Exhibit Postnatal Lethality

Richard J. Davis,1 Weiping Shen,2 Yakov I. Sandler,3 Mehran Amoui,4 Patricia Purcell,5 Richard Maas,5 Ching-Nan Ou,1 Hannes Vogel,1 Arthur L. Beaudet,6 and Graeme Mardon1,3,6,7,8,*

Departments of Pathology,1 Neuroscience,3 Ophthalmology,6 and Molecular and Human Genetics7 and Program in Developmental Biology,8 Baylor College of Medicine, and Department of Pathology, M. D. Anderson Cancer Center,2 Houston, Texas 77030; Department of Physiology and Biophysics, Health Sciences Center, University of New York at Stony Brook, Stony Brook, New York 117944; and Genetics Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 021155

Received 13 November 2000/Accepted 27 November 2000

Drosophila dachshund is necessary and sufficient for compound eye development and is required for normal leg and brain development. A mouse homologue of dachshund, Dach1, is expressed in the developing retina and limbs, suggesting functional conservation of this gene. We have generated a loss-of-function mutation in Dach1 that results in the abrogation of the wild-type RNA and protein expression pattern in embryos. Homozygous mutants survive to birth but exhibit postnatal lethality associated with a failure to suckle, cyanosis, and respiratory distress. The heart, lungs, kidneys, liver, and skeleton were examined to identify factors involved in postnatal lethality, but these organs appeared to be normal. In addition, blood chemistry tests failed to reveal differences that might explain the lethal phenotype. Gross examination and histological analyses of newborn eyes, limbs, and brains revealed no detectable abnormalities. Since Dach1 mutants die shortly after birth, it remains possible that Dach1 is required for postnatal development of these structures. Alternatively, an additional Dach homologue may functionally compensate for Dach1 loss of function.

* Corresponding author. Mailing address: Department of Pathology, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030. Phone: (713) 798-8731. Fax: (713) 798-3359. E-mail: gmardon{at}bcm.tmc.edu.

Molecular and Cellular Biology, March 2001, p. 1484-1490, Vol. 21, No. 5
0270-7306/01/$04.00+0   DOI: 10.1128/MCB.21.5.1484-1490.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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