- THIS ARTICLE
- Full Text
- Full Text (PDF)
- Alert me when this article is cited
- Alert me if a correction is posted
- SERVICES
- 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 Malmanche, N.
- Articles by Clark, D. V.
- Search for Related Content
- PUBMED
- PubMed Citation
- Articles by Malmanche, N.
- Articles by Clark, D. V.
Genetics, Vol. 168, 2011-2023, December 2004, Copyright © 2004
doi:10.1534/genetics.104.033134
Drosophila melanogaster Prat, a Purine de Novo Synthesis Gene, Has a Pleiotropic Maternal-Effect Phenotype
Nicolas Malmanche1 and Denise V. Clark2
Department of Biology, University of New Brunswick, Fredericton, New Brunswick E3B 6E1, Canada
2 Corresponding author: Department of Biology, University of New Brunswick, 10 Bailey Dr., Fredericton, NB E3B 5A3, Canada.
E-mail: clarkd{at}unb.ca
In Drosophila melanogaster, two genes, Prat and Prat2, encode the enzyme, amidophosphoribosyltransferase, that performs the first and limiting step in purine de novo synthesis. Only Prat mRNA is present in the female germline and 0- to 2-hr embryos prior to the onset of zygotic transcription. We studied the maternal-effect phenotype caused by Prat loss-of-function mutations, allowing us to examine the effects of decreased purine de novo synthesis during oogenesis and the early stages of embryonic development. In addition to the purine syndrome previously characterized, we found that Prat mutant adult females have a significantly shorter life span and are conditionally semisterile. The semisterility is associated with a pleiotropic phenotype, including egg chamber defects and later effects on embryonic and larval viability. Embryos show mitotic synchrony and/or nuclear content defects at the syncytial blastoderm stages and segmentation defects at later stages. The semisterility is partially rescued by providing Prat mutant females with an RNA-enriched diet as a source of purines. Our results suggest that purine de novo synthesis is a limiting factor during the processes of cellular or nuclear proliferation that take place during egg chamber and embryonic development.
This article has been cited by other articles:
 |
|
 |
|
  W. Wang, C. Cronmiller, and D. L. Brautigan Maternal Phosphatase Inhibitor-2 Is Required for Proper Chromosome Segregation and Mitotic Synchrony During Drosophila Embryogenesis Genetics, August 1, 2008; 179(4): 1823 - 1833. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. J. Wittkopp, B. K. Haerum, and A. G. Clark Parent-of-Origin Effects on mRNA Expression in Drosophila melanogaster Not Caused by Genomic Imprinting Genetics, July 1, 2006; 173(3): 1817 - 1821. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
Y. Ji and D. V. Clark The Purine Synthesis Gene Prat2 Is Required for Drosophila Metamorphosis, as Revealed by Inverted-Repeat-Mediated RNA Interference Genetics, March 1, 2006; 172(3): 1621 - 1631. [Abstract] [Full Text] [PDF]
|
|