A Mutation With Major Effects on Drosophila melanogaster Sex Pheromones

Author:

Marcillac Fabrice1,Bousquet François1,Alabouvette Josiane1,Savarit Fabrice2,Ferveur Jean-François1

Affiliation:

1. Unité de Recherche 5548 Associée au Centre National de la Recherche Scientifique, Faculté des Sciences, Université de Bourgogne, 21000 Dijon, France and

2. LEEC, CNRS-FRE 2413, Université de Paris 13, 93430 Villetaneuse, France

Abstract

Abstract Sex pheromones are intraspecific chemical signals that are crucial for mate attraction and discrimination. In Drosophila melanogaster, the predominant hydrocarbons on the cuticle of mature female and male flies are radically different and tend to stimulate or inhibit male courtship, respectively. This sexual difference depends largely upon the number of double bonds (one in males and two in females) added by desaturase enzymes. A mutation was caused by a PGal4 transposon inserted in the desat1 gene that codes for the desaturase crucial for setting these double bonds. Homozygous mutant flies produced 70–90% fewer sex pheromones than control flies, and the pheromonal difference between the sexes was almost abolished. A total of 134 excision alleles were induced by pulling out all or a part of the transposon. The pheromonal profile was generally rescued in excision alleles with a completely or largely removed transposon whereas it remained mutant in alleles with a larger piece of the transposon. Five desat1 transcripts were detected during larval-to-adult development. Their levels were precisely quantified in 24-hr-old adults, a critical period for the production of sex pheromones. Three transcripts significantly varied between control females and males; however, the predominant transcript showed no difference. In mutant flies, the predominant transcript was highly decreased with the two sexually dimorphic transcripts.These two transcripts were also absent in the sibling species D. simulans, which shows no sexually dimorphic hydrocarbons. We also induced a larval-lethal allele that lacked all transcripts and failed to complement the defective hydrocarbon phenotype of mutant alleles.

Publisher

Oxford University Press (OUP)

Subject

Genetics

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