Genetic analysis of viable and lethalfused mutants ofDrosophila melanogaster

Abstract

Fused is a segmentation gene belonging to the segment-polarity class. Mutations at thefused locus are known to display pleiotropic effects, causing zygotically determined anomalies of ovaries and of some adult cuticular structures, and maternally determined embryonic segmentation defects. In order to determine the amorphic phenotype offused and to study the genetical basis of its pleiotropy, newfused alleles (18 viable and 11 lethal) were isolated. The phenotype of these mutants and of others already known are described, taking into account zygotic and maternal effects. The main results provided by this analysis are as follows. Firstly, allfused alleles show the whole complex fused phenotype, and a good correlation is observed between the strength of the wing and segmentation defects, suggesting that a single function is involved in both processes. Secondly, all embryonic and larval lethals carry deficiencies which allow us to localizefused between the 17C4 and 17D2 bands of the X-chromosome. Thirdly, the 24 viable and 2 pupal lethals examined behave as point mutants, as shown cytologically or by Southern blot analysis. However, only one of them, the pupal lethalfu was proven to carry a nullfused allele, since it displays in germ-line clones a strong maternal phenotype and a very low zygotic rescue, similar to those of the small deficiencyDf(1)fu. The phenotype of the amorphic mutant indicates that zygotic ezpression offused is required for normal metamorphosis, while maternal expression is necessary for a normal segmentation pattern, since a complete loss offused expression during oogenesis cannot be compensated zygotically.

fused regulates germline cyst mitosis and differentiation during Drosophila oogenesis

“…1F). The proportion of ovarioles with tumorous follicles as assayed by DAPI staining varied significantly depending on the allele (from 7 to 85%) and could be correlated with the fecundity reported for the allele (Busson et al, 1988). However, it was not possible to correlate the severity of the tumorous phenotype with the class of fu allele since each class contains fu alleles associated with both strong and weaker penetrance for this phenotype (Fig.…”

“…Several fu alleles described in Busson et al (1988) were analyzed: fu 1 and fu JB3 belong to class I alleles, fu A and fu G3 belong to class II alleles, fu Z4 to class 0 alleles. Class I and class II alleles were identified genetically (Therond et al, 1996).…”

“…Mutations in the fused (fu) gene, which encodes a serine/threonine kinase previously identified as a positive effector of the Hedgehog (Hh) signal transduction pathway in Drosophila embryonic and imaginal disc development (Alves et al, 1998;Ingham, 1993;Limbourg-Bouchon et al, 1991;Sanchez-Herrero et al, 1996), are also associated with the production of poorly-characterized ovarian germline tumors (Bopp et al, 1993;Busson et al, 1988;King, 1970;Oliver et al, 1993). Although we have previously shown a role during oogenesis for Fu-dependent classical Hh signal transduction for somatic cell differentiation during follicle formation (Besse et al, 2002), fu is the only component of Hedgehog signaling whose mutations give rise to an ovarian tumor phenotype (Besse et al, 2002;Forbes et al, 1996a,b;Vied and Horabin, 2001;Besse and Pret, unpublished results).…”

Morphogenetic Apoptosis: A Mechanism for Correcting Discontinuities in Morphogen Gradients

“…P1 , puc-lacZ E69 , brk-lacZ 3sB , and dpp blk -Gal4 lines have been described previously (Sun et al, 1995;Martín-Blanco et al, 1998;Minami et al, 1999) and tkv a12 mutations (Busson et al, 1988;Glise et al, 1995;Adachi-Yamada et al, 1999).…”

Hedgehog signaling and the axial patterning ofDrosophilawings

“…This has been interpreted as meaning that Su(Fu) may only act in opposition to the function of Fu. Mutations in fu cause a reduction or loss of the 3/4 intervein resulting from decreased levels of Hh signaling Busson et al 1988;Sanchez-Herrero et al 1996). The levels of Ci-155 in fu and su(fu), mutants offer an explanation to the apparent paradox that while Ci-155 is thought to be a transcriptional activator, its cellular distribution is largely cytoplasmic.…”