- THIS ARTICLE
- Full Text
- Full Text (PDF)
- Data Supplement
-
All Versions of this Article:
genetics.107.072280v1
177/1/239 most recent - Alert me when this article is cited
- Alert me if a correction is posted
- SERVICES
- Email this article to a friend
- Similar articles in this journal
- Similar articles in PubMed
- Alert me to new issues of the journal
- Download to citation manager
- Reprints & Permissions
- CITING ARTICLES
- Citing Articles via HighWire
- Citing Articles via Google Scholar
- GOOGLE SCHOLAR
- Articles by Acevedo, S. F.
- Articles by Skoulakis, E. M. C.
- Search for Related Content
- PUBMED
- PubMed Citation
- Articles by Acevedo, S. F.
- Articles by Skoulakis, E. M. C.
Originally published as Genetics Published Articles Ahead of Print on July 29, 2007.
Genetics, Vol. 177, 239-253, September 2007, Copyright © 2007
doi:10.1534/genetics.107.072280
In Vivo Functional Specificity and Homeostasis of Drosophila 14-3-3 Proteins
Summer F. Acevedo1,2, K. Kirki Tsigkari1, Sofia Grammenoudi and Efthimios M. C. Skoulakis3
Institute of Molecular Biology and Genetics, Biomedical Sciences Research Centre "Alexander Fleming," 16672 Vari, Greece
3 Corresponding author: Institute of Molecular Biology and Genetics, Biomedical Sciences Research Centre "Alexander Fleming," 34 Fleming Str., 16672 Vari, Greece.
E-mail: skoulakis{at}fleming.gr
The functional specialization or redundancy of the ubiquitous 14-3-3 proteins constitutes a fundamental question in their biology and stems from their highly conserved structure and multiplicity of coexpressed isotypes. We address this question in vivo using mutations in the two Drosophila 14-3-3 genes, leonardo (14-3-3
) and D14-3-3
. We demonstrate that D14-3-3 is essential for embryonic hatching. Nevertheless, D14-3-3 null homozygotes survive because they upregulate transcripts encoding the LEOII isoform at the time of hatching, compensating D14-3-3 loss. This novel homeostatic response explains the reported functional redundancy of the Drosophila 14-3-3 isotypes and survival of D14-3-3 mutants. The response appears unidirectional, as D14-3-3 elevation upon LEO loss was not observed and elevation of leo transcripts was stage and tissue specific. In contrast, LEO levels are not changed in the wing disks, resulting in the aberrant wing veins characterizing D14-3-3 mutants. Nevertheless, conditional overexpression of LEOI, but not of LEOII, in the wing disk can partially rescue the venation deficits. Thus, excess of a particular LEO isoform can functionally compensate for D14-3-3 loss in a cellular-context-specific manner. These results demonstrate functional differences both among Drosophila 14-3-3 proteins and between the two LEO isoforms in vivo, which likely underlie differential dimer affinities toward 14-3-3 targets.
This article has been cited by other articles:
 |
|
 |
|
  C. Temme, R. Weissbach, H. Lilie, C. Wilson, A. Meinhart, S. Meyer, R. Golbik, A. Schierhorn, and E. Wahle The Drosophila melanogaster Gene cg4930 Encodes a High Affinity Inhibitor for Endonuclease G J. Biol. Chem., March 27, 2009; 284(13): 8337 - 8348. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. Moressis, A. R. Friedrich, E. Pavlopoulos, R. L. Davis, and E. M. C. Skoulakis A Dual Role for the Adaptor Protein DRK in Drosophila Olfactory Learning and Memory J. Neurosci., February 25, 2009; 29(8): 2611 - 2625. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. M. A. Moreira, T. Shen, G. Ohlsson, P. Gromov, I. Gromova, and J. E. Celis A Combined Proteome and Ultrastructural Localization Analysis of 14-3-3 Proteins in Transformed Human Amnion (AMA) Cells: Definition of A Framework to Study Isoform-Specific Differences Mol. Cell. Proteomics, July 1, 2008; 7(7): 1225 - 1240. [Abstract] [Full Text] [PDF]
|
|
|