help button home button Genetics Journal Watch
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Originally published as Genetics Published Articles Ahead of Print on July 5, 2005.

Genetics, Vol. 171, 597-614, October 2005, Copyright © 2005
doi:10.1534/genetics.105.045021

This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Supplemental Data
Right arrow All Versions of this Article:
genetics.105.045021v1
171/2/597    most recent
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 arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Coelho, C. M. A.
Right arrow Articles by Marygold, S. J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Coelho, C. M. A.
Right arrow Articles by Marygold, S. J.

A Genetic Screen for Dominant Modifiers of a Small-Wing Phenotype in Drosophila melanogaster Identifies Proteins Involved in Splicing and Translation

Carmen M. A. Coelho, Benjamin Kolevski, Cherryl D. Walker, Irene Lavagi, Thomas Shaw, Anselm Ebert, Sally J. Leevers1 and Steven J. Marygold

Growth Regulation Laboratory, Cancer Research UK London Research Institute, London WC2A 3PX, United Kingdom

1 Corresponding author: Growth Regulation Laboratory, Cancer Research UK London Research Institute, 44 Lincoln's Inn Fields, London WC2A 3PX, United Kingdom.
E-mail: sally.leevers{at}cancer.org.uk

Studies in the fly, Drosophila melanogaster, have revealed that several signaling pathways are important for the regulation of growth. Among these, the insulin receptor/phosphoinositide 3-kinase (PI3K) pathway is remarkable in that it affects growth and final size without disturbing pattern formation. We have used a small-wing phenotype, generated by misexpression of kinase-dead PI3K, to screen for novel mutations that specifically disrupt organ growth in vivo. We identified several complementation groups that dominantly enhance this small-wing phenotype. Meiotic recombination in conjunction with visible markers and single-nucleotide polymorphisms (SNPs) was used to map five enhancers to single genes. Two of these, nucampholin and prp8, encode pre-mRNA splicing factors. The three other enhancers encode factors required for mRNA translation: pixie encodes the Drosophila ortholog of yeast RLI1, and RpL5 and RpL38 encode proteins of the large ribosomal subunit. Interestingly, mutations in several other ribosomal protein-encoding genes also enhance the small-wing phenotype used in the original screen. Our work has therefore identified mutations in five previously uncharacterized Drosophila genes and provides in vivo evidence that normal organ growth requires optimal regulation of both pre-mRNA splicing and mRNA translation.




This article has been cited by other articles:


Home page
 GeneticsHome page
J. Z. Morris, L. Bergman, A. Kruyer, M. Gertsberg, A. Guigova, R. Arias, and M. Pogorzelska
Mutations in the Drosophila Mitochondrial tRNA Amidotransferase, bene/gatA, Cause Growth Defects in Mitotic and Endoreplicating Tissues
Genetics, February 1, 2008; 178(2): 979 - 987.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
Z.-q. Chen, J. Dong, A. Ishimura, I. Daar, A. G. Hinnebusch, and M. Dean
The Essential Vertebrate ABCE1 Protein Interacts with Eukaryotic Initiation Factors
J. Biol. Chem., March 17, 2006; 281(11): 7452 - 7457.
[Abstract] [Full Text] [PDF]

Home page
 DevelopmentHome page
C. M. A. Coelho, B. Kolevski, C. Bunn, C. Walker, A. Dahanukar, and S. J. Leevers
Growth and cell survival are unevenly impaired in pixie mutant wing discs
Development, December 15, 2005; 132(24): 5411 - 5424.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 2005 by the Genetics Society of America.