Author
Listed:
- Aaron DiAntonio
(Washington University School of Medicine, 660 S. Euclid, Campus Box 8103)
- Ali P. Haghighi
(University of California, Berkeley, Room 509 Life Sciences Addition)
- Scott L. Portman
(Washington University School of Medicine, 660 S. Euclid, Campus Box 8103)
- Jason D. Lee
(University of California, Berkeley, Room 509 Life Sciences Addition)
- Andrew M. Amaranto
(Washington University School of Medicine, 660 S. Euclid, Campus Box 8103)
- Corey S. Goodman
(University of California, Berkeley, Room 509 Life Sciences Addition)
Abstract
The covalent attachment of ubiquitin to cellular proteins is a powerful mechanism for controlling protein activity and localization1. Ubiquitination is a reversible modification promoted by ubiquitin ligases and antagonized by deubiquitinating proteases2. Ubiquitin-dependent mechanisms regulate many important processes including cell-cycle progression, apoptosis and transcriptional regulation3. Here we show that ubiquitin-dependent mechanisms regulate synaptic development at the Drosophila neuromuscular junction (NMJ). Neuronal overexpression of the deubiquitinating protease fat facets4 leads to a profound disruption of synaptic growth control; there is a large increase in the number of synaptic boutons, an elaboration of the synaptic branching pattern, and a disruption of synaptic function. Antagonizing the ubiquitination pathway in neurons by expression of the yeast deubiquitinating protease UBP2 (ref. 5) also produces synaptic overgrowth and dysfunction. Genetic interactions between fat facets and highwire6, a negative regulator of synaptic growth that has structural homology to a family of ubiquitin ligases, suggest that synaptic development may be controlled by the balance between positive and negative regulators of ubiquitination.
Suggested Citation
Aaron DiAntonio & Ali P. Haghighi & Scott L. Portman & Jason D. Lee & Andrew M. Amaranto & Corey S. Goodman, 2001.
"Ubiquitination-dependent mechanisms regulate synaptic growth and function,"
Nature, Nature, vol. 412(6845), pages 449-452, July.
Handle:
RePEc:nat:nature:v:412:y:2001:i:6845:d:10.1038_35086595
DOI: 10.1038/35086595
Download full text from publisher
As the access to this document is restricted, you may want to search for a different version of it.
Corrections
All material on this site has been provided by the respective publishers and authors. You can help correct errors and omissions. When requesting a correction, please mention this item's handle: RePEc:nat:nature:v:412:y:2001:i:6845:d:10.1038_35086595. See general information about how to correct material in RePEc.
If you have authored this item and are not yet registered with RePEc, we encourage you to do it here. This allows to link your profile to this item. It also allows you to accept potential citations to this item that we are uncertain about.
We have no bibliographic references for this item. You can help adding them by using this form .
If you know of missing items citing this one, you can help us creating those links by adding the relevant references in the same way as above, for each refering item. If you are a registered author of this item, you may also want to check the "citations" tab in your RePEc Author Service profile, as there may be some citations waiting for confirmation.
For technical questions regarding this item, or to correct its authors, title, abstract, bibliographic or download information, contact: Sonal Shukla or Springer Nature Abstracting and Indexing (email available below). General contact details of provider: http://www.nature.com .
Please note that corrections may take a couple of weeks to filter through
the various RePEc services.