This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Simon, R.
Right arrow Articles by Lufkin, T.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Simon, R.
Right arrow Articles by Lufkin, T.

 Previous Article  |  Next Article 

Molecular and Cellular Biology, December 2003, p. 9046-9060, Vol. 23, No. 24
0270-7306/03/$08.00+0     DOI: 10.1128/MCB.23.24.9046-9060.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

Postnatal Lethality in Mice Lacking the Sax2 Homeobox Gene Homologous to Drosophila S59/slouch: Evidence for Positive and Negative Autoregulation

Ruth Simon and Thomas Lufkin*

Brookdale Center for Developmental and Molecular Biology, Mount Sinai School of Medicine, New York, New York 10029-6574

Received 2 July 2003/ Returned for modification 20 August 2003/ Accepted 18 September 2003

Homeobox gene transcription factors direct multiple functions during development. They are involved in early patterning of the embryo as well as cell specification, cell differentiation, and organogenesis. Here we describe a previously uncharacterized murine homeobox gene, Sax2, that shows high similarity to the Drosophila S59/slouch and murine Sax1 genes. We show that Sax2 gene expression occurs early during embryogenesis in the midbrain, the midbrain-hindbrain boundary, the ventral neural tube, the developing eye, and the apical ectodermal ridge of the limb. To determine the role of Sax2 during development, we generated a knockout mouse line by replacing part of the Sax2 coding sequences with the lacZ gene. The Sax2 null allele mutants exhibit a strong phenotype indicated by growth retardation starting immediately after birth and leading to premature death within the first 3 weeks postnatal. Intriguingly, our studies also demonstrated a striking autoregulation of the Sax2 gene in both positive- and negative-feedback mechanisms depending on the specific cell type expressing Sax2.


* Corresponding author. Mailing address: Brookdale Center for Developmental and Molecular Biology, Mount Sinai School of Medicine, Box 1020, One Gustave L. Levy Place, New York, NY 10029-6574. Phone: (212) 241-5359. Fax: (212) 214-0873. E-mail: thomas.lufkin{at}mssm.edu.


Molecular and Cellular Biology, December 2003, p. 9046-9060, Vol. 23, No. 24
0022-538X/03/$08.00+0     DOI: 10.1128/MCB.23.24.9046-9060.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.




This article has been cited by other articles:

  • Schubert, F. R., Lumsden, A. (2005). Transcriptional control of early tract formation in the embryonic chick midbrain. Development 132: 1785-1793 [Abstract] [Full Text]