Genetics, Vol. 157, 751-764, February 2001, Copyright © 2001

Comparative Analysis of the nonA Region in Drosophila Identifies a Highly Diverged 5' Gene That May Constrain nonA Promoter Evolution

Susanna Campesana, David Chalmersa, Federica Sandrellib, Aram Megighianc, Alexandre A. Peixotoa,d, Rodolfo Costab, and Charalambos P. Kyriacoua
a Department of Genetics, University of Leicester, Leicester LE1 7RH, England,
b Dipartimento di Biologia, Università di Padova, 35131 Padova, Italy,
c Dipartimento di Anatomia e Fisiologia Umana, Università di Padova, 35131, Padova, Italy
d Departamento de Bioquimica e Biologia Molecular, Fundacao Oswaldo Cruz, Rio de Janeiro, CEP 21045-900, Brazil

Corresponding author: Charalambos P. Kyriacou, Department of Genetics, University of Leicester, Leicester LE1 7RH, United Kingdom., cpk{at}leicester.ac.uk (E-mail)

Communicating editor: J. J. LOROS

A genomic fragment from Drosophila virilis that contained all the no-on-transientA (nonA) coding information, plus several kilobases of upstream material, was identified. Comparisons of nonA sequences and the gene nonA-like in D. melanogaster, a processed duplication of nonA, suggest that it arose before the split between D. melanogaster and D. virilis. In both species, another gene that lies <350 bp upstream from the nonA transcription starts, and that probably corresponds to the lethal gene l(1)i19, was identified. This gene encodes a protein that shows similarities to GPI1, which is required for the biosynthesis of glycosylphosphatidylinositol (GPI), a component for anchoring eukaryotic proteins to membranes, and so we have named it dGpi1. The molecular evolution of nonA and dGpi1 sequences show remarkable differences, with the latter revealing a level of amino acid divergence that is as high as that of transformer and with extremely low levels of codon bias. Nevertheless, in D. melanogaster hosts, the D. virilis fragment rescues the lethality associated with a mutation of l(1)i19e, as well as the viability and visual defects produced by deletion of nonA-. The presence of dGpi1 sequences so close to nonA appears to have constrained the evolution of the nonA promoter.





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