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 Wesley, C. S.
Right arrow Articles by Mok, L.-P.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Wesley, C. S.
Right arrow Articles by Mok, L.-P.

 Previous Article  |  Next Article 

Molecular and Cellular Biology, August 2003, p. 5581-5593, Vol. 23, No. 16
0270-7306/03/$08.00+0     DOI: 10.1128/MCB.23.16.5581-5593.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

Regulation of Notch Signaling by a Novel Mechanism Involving Suppressor of Hairless Stability and Carboxyl Terminus-Truncated Notch

Cedric S. Wesley* and Lee-Peng Mok

Department of Microbiology and Molecular Genetics, The University of Vermont, Burlington, Vermont 05405

Received 12 December 2002/ Returned for modification 26 February 2003/ Accepted 20 May 2003

Different amounts of Suppressor of Hairless (SuH)-dependent Notch (N) signaling is often used during animal development to produce two different tissues from a population of equipotent cells. During Drosophila melanogaster embryogenesis, cells with high amounts of this signaling differentiate the larval epidermis whereas cells with low amounts, or none, differentiate the central nervous system (CNS). The mechanism by which SuH-dependent N signaling is increased or decreased in these different cells is obscure. The developing epidermis is known to get enriched for the full-length N (NFull) and the developing CNS for the carboxyl terminus-truncated N (N{Delta}Cterm). Results described here indicate that this differential accumulation of N receptors is part of a mechanism that would promote SuH-dependent N signaling in the developing epidermis but suppress it in the developing CNS. This mechanism involves SuH-dependent stability of NFull, NFull-dependent accumulation of SuH, stage specific stability of SuH, and N{Delta}Cterm-dependent loss of SuH and NFull.


* Corresponding author. Mailing address: Department of Microbiology and Molecular Genetics, 322 Stafford Hall, 95 Carrigan Dr., The University of Vermont, Burlington, VT 05405. Phone: (802) 656-8024. Fax: (802) 656-8749. E-mail: cwesley{at}zoo.uvm.edu.


Molecular and Cellular Biology, August 2003, p. 5581-5593, Vol. 23, No. 16
0022-538X/03/$08.00+0     DOI: 10.1128/MCB.23.16.5581-5593.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.




This article has been cited by other articles:

  • Ahimou, F., Mok, L.-P., Bardot, B., Wesley, C. (2004). The adhesion force of Notch with Delta and the rate of Notch signaling. JCB 167: 1217-1229 [Abstract] [Full Text]