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 Parrish, M.
Right arrow Articles by Monaghan, A. P.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Parrish, M.
Right arrow Articles by Monaghan, A. P.

 Previous Article  |  Next Article 

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.

Loss of the Sall3 Gene Leads to Palate Deficiency, Abnormalities in Cranial Nerves, and Perinatal Lethality

M. Parrish,1,{dagger} T. Ott,2,{dagger} 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 mice—Spalt1 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.


* Corresponding author. Mailing address: W1455 BST, 3500 Terrace St., Pittsburgh, PA 15261. Phone: (412) 648-1856. Fax: (412) 648-1441. E-mail: monaghan{at}pitt.edu.

{dagger} M.P. and T.O. contributed equally to this work.


Molecular and Cellular Biology, August 2004, p. 7102-7112, Vol. 24, No. 16
0022-538X/04/$08.00+0     DOI: 10.1128/MCB.24.16.7102-7112.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.




This article has been cited by other articles:

  • Giovannone, B., Tsiaras, W. G., de la Monte, S., Klysik, J., Lautier, C., Karashchuk, G., Goldwurm, S., Smith, R. J. (2009). GIGYF2 gene disruption in mice results in neurodegeneration and altered insulin-like growth factor signaling. Hum Mol Genet 18: 4629-4639 [Abstract] [Full Text]  
  • Shikauchi, Y., Saiura, A., Kubo, T., Niwa, Y., Yamamoto, J., Murase, Y., Yoshikawa, H. (2009). SALL3 Interacts with DNMT3A and Shows the Ability To Inhibit CpG Island Methylation in Hepatocellular Carcinoma. Mol. Cell. Biol. 29: 1944-1958 [Abstract] [Full Text]  
  • Kawakami, Y., Uchiyama, Y., Rodriguez Esteban, C., Inenaga, T., Koyano-Nakagawa, N., Kawakami, H., Marti, M., Kmita, M., Monaghan-Nichols, P., Nishinakamura, R., Izpisua Belmonte, J. C. (2009). Sall genes regulate region-specific morphogenesis in the mouse limb by modulating Hox activities. Development 136: 585-594 [Abstract] [Full Text]  
  • Palmieri, C., Loi, P., Ptak, G., Salda, L.D. (2008). REVIEW PAPER: A Review of the Pathology of Abnormal Placentae of Somatic Cell Nuclear Transfer Clone Pregnancies in Cattle, Sheep, and Mice. Vet Pathol 45: 865-880 [Abstract] [Full Text]  
  • Sakaki-Yumoto, M., Kobayashi, C., Sato, A., Fujimura, S., Matsumoto, Y., Takasato, M., Kodama, T., Aburatani, H., Asashima, M., Yoshida, N., Nishinakamura, R. (2006). The murine homolog of SALL4, a causative gene in Okihiro syndrome, is essential for embryonic stem cell proliferation, and cooperates with Sall1 in anorectal, heart, brain and kidney development. Development 133: 3005-3013 [Abstract] [Full Text]  
  • Harvey, S. A., Logan, M. P. O. (2006). sall4 acts downstream of tbx5 and is required for pectoral fin outgrowth.. Development 133: 1165-1173 [Abstract] [Full Text]