Complementation between alleles at the ovarian tumor locus of Drosophila melanogaster

Abstract

The (ovarian tumor) otu gene resides at 23.2 on the genetic map of the X chromosome and near 7F1 on the cytological map. This germ line-expressed locus behaves as if it encodes a gene product which is required during certain steps in the transformation of oogonia into functional oocytes. On the basis of their ovarian morphologies 17 ethyl methane sulfonate (EMS)-induced mutants have been distributed among three developmental classes as follows: quiescent (eight), oncogenic (four), and differentiated (five). The otu13 and otu14 alleles interact to yield fertile females, and many other heteroallelic combinations show partial complementation. Since many mutant alleles interact beneficially, the functional product of the otu gene may be a multimer. We conclude, from an analysis of heteroallelic interactions and dosage effects, that the abnormal phenotypes observed are graded consequences of reduced levels of functional gene product and that the minimum concentration required for development increases as oogenesis proceeds.

Enhanced cost of mating in female sterile mutants of Drosophila melanogaster.

“…The phenotype of the otu mutants are known to vary depending on different alleles. According to the affected stages in oogenesis, they are classified into three groups; quiescent alleles (QUI) in which germ cells are lacking, oncogenic alleles (ONC) which are defective in the proliferation of germ cells, and differentiating alleles (DIF) which are defective in nurse cell/oocyte differentiation (King et al, 1986;Storto and King, 1988 , used in the present study are one of QUI, ONC and DIF alleles, respectively. Despite such heterogeneity in the stages at which oogenesis was arrested, the life-shortening effect of mating was similar across the otu allels, indicating that the stages of oogenesis attained have little effect on the cost of mating.…”

“…To sterilize the females, three different alleles of a female sterile mutant, ovarian tumor ( otu ), were used. The oogenesis of homozygous otu females arrests at various stages, depending on the alleles (King et al, 1986;Storto and King, 1988). In addition, we tested another female sterile mutant, dunce ( dnc ), of which the effect of mating on female longevity has previously been reported (Bellen and Kiger, 1987;Chapman et al, 1996).…”

A specific ovarian tumor protein isoform is required for efficient differentiation of germ cells in Drosophila oogenesis.

“…The otu gene is a potentially promising candidate for a molecular analysis of oogenesis, because otu mutants display a remarkable range of ovarian pathologies. Seventeen ethylmethane sulfonate (EMS)-induced, and 13 P-element-induced, or P-element-derived, otu mutants have been recovered (Gans et al 1975;Mohler 1977;Digan 1980;King and Riley 1982;King et al 1986;Mulligan et al 1988;G. Sass and D. Mohler, unpubl.).…”

“…Sass and D. Mohler, unpubl.). The phenotypes displayed by otu mutants are divided into three developmental classes that highlight specific steps within oogenesis which may be affected by or under the control of the otu gene (King et al 1986). An otu mutant is classified by the predominant phenotype displayed within the ovary; however, multiple phenotypes may be present in any given ovary.…”

“…Cystocyte divisions are not always precise, and some alleles exhibit odd numbers of nurse cells or no oocyte. Those egg chambers that contain oocytes usually proceed through oogenesis to what has been called a "pseudo-12" (pi2) stage but do not complete development (King et al 1986;Storto and King 1988).…”