Broad‐Complex function during oogenesis in <i>Drosophila melanogaster</i>

Huang, Ruea-Yea; Orr, William C.

doi:10.1002/dvg.1020130405

Cited by 14 publications

(7 citation statements)

References 43 publications

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“…X-Gal staining was observed in salivary glands, fat body, Malpighian tubules, gut, and brain during the third instar. Very specific traits, such as dotted expression in maxillary palps in late pupae, in agreement with the reduced bristles on palpus (rbp) phenotype (Kiss et al 1988), and expression in ovarian follicular cells, in agreement with the sterility and egg shell defects observed in some BRC mutants (Mazina et al 1991;Huang and Orr 1992), were observed (a detailed account will be published elsewhere). Considering what is presently known from molecular studies on the BRC temporal and tissular expression (Huet et al 1993;Karim et al 1993;Emery et al 1994}, the observed lacZ pattern in convertants can be interpreted as a partial image of the BRC expression.…”

Section: The Enhancer-trap Expression Patternsupporting

confidence: 56%

Enhancer-trap targeting at the Broad-Complex locus of Drosophila melanogaster.

Gonzy‐Tréboul¹,

Lepesant²,

Deutsch³

1995

Genes Dev.

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Here, we describe the exact replacement of a defective unmarked P element by an enhancer-trap transposon marked by the miniwhite gene and carrying lacZ as a reporter gene. The original defective P element was located in an intron of the Broad-Complex (BRC), a key gene involved in metamorphosis. Replacement events resulted from conversions induced by the P-element transposase from a donor enhancer-trap element located on another chromosome. Six independent conversion events were selected. In all converted chromosomes, the enhancer-trap transposon was in the same orientation as the original P element. From the pattern of X-gal staining observed, lacZ expression likely reflects the regulatory influence of BRC enhancers on the convertant transposon. Reversion to wild type was achieved by excision of the enhancer-trap transposon. The six convertants were analyzed in detail at the nucleotide level. The occurrence of a polymorphism at position 33 of the P-element sequences led us to propose a conversion mechanism involving homologous P sequences for repair. This is in contrast to previously analyzed P-element transposase-induced conversion events and proposed models relying on sequence identity between genomic Drosophila sequences. The lack of any homology requirement other than between P element sequences means that our findings can be easily generalized. Targeting a marked P-element derivative at a precise site without loss or addition of genetic information makes it possible to exploit the hundreds of defective P elements scattered throughout the Drosophila genome by replacing them with engineered P elements, already available.[Key Words: Enhancer-trap; P element; conversion; homologous recombination; Broad-Complex; Drosophila] Received November 14, 1994; revised version accepted March 23, 1995.For -12 years, P-element derivatives have been used extensively as vectors for germ-line transformation (Rubin and Spradling 1982) and enhancer trapping (O'Kane and Gehring 1987). Unlike yeast molecular genetics with its system of transformation and mouse molecular genetics with its system of transgenesis, Drosophila molecular genetics suffers from the lack of a genetic system that permits easy selection of homologous recombination events. In vitro-engineered P elements containing Drosophila sequences do not reach the original genomic site of these sequences but, rather, insert at any location in the genome, although some homing effects, not fully understood yet, have been reported in certain conditions (Fauvarque and Dura 1993;Hama et al. 1990). This random insertion of P elements generates position effects that result from unrelated flanking sequences. The development of enhancer-detector elements turned this drawback into an advantage (for review, see Wilson et al. 1990). In these elements, a lacZ reporter gene is fused to a weak Drosophila-compatible promoter, the P element promoter itself. Insertion of the enhancer-detector element near flanking Drosophila genomic enhancers can activate this promoter, thus allowing th...

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Section: The Enhancer-trap Expression Patternsupporting

confidence: 56%

Enhancer-trap targeting at the Broad-Complex locus of Drosophila melanogaster.

Gonzy‐Tréboul¹,

Lepesant²,

Deutsch³

1995

Genes Dev.

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“…The Z1 isoform of BR-C becomes expressed in the patches of follicular cells destined to form the dorsal appendages, and may be an upstream regulator of this process (Huang and Orr, 1992;Deng and Bownes, 1997).…”

Section: Chorion Genes and Regulation Of Chorion Gene Expression P0935mentioning

confidence: 99%

Vitellogenesis and Post-Vitellogenic Maturation of the Insect Ovarian Follicle

Swevers

2005

Comprehensive Molecular Insect Science

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“…BRC mutants have common and complementation group-restricted phenotypes (Kiss et al 1988;White 1991, 1992;Huang and Orr 1992;Karim et al 1993;O'Keefe et al 1995;Sandstrom et al 1997;Liu and Restifo 1998;Mugat et al 2000;Brennan et al 2001;Consoulas et al 2005;Wilson et al 2006). Molecularly, BRC consists of a common 5′ exon, encoding a protein-binding region called BRcore, that is alternatively spliced to one of four tandemly duplicated 3′ exons, encoding zinc-finger-motif DNA-binding domains Z1, Z2, Z3, and Z4 (DiBello et al 1991;Bayer et al 1996).…”

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confidence: 98%

Anciently duplicated Broad Complex exons have distinct temporal functions during tissue morphogenesis

Spokony

Restifo

2007

Dev Genes Evol

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Broad Complex (BRC) is an essential ecdysone-pathway gene required for entry into and progression through metamorphosis in Drosophila melanogaster. Mutations of three BRC complementation groups cause numerous phenotypes, including a common suite of morphogenesis defects involving central nervous system (CNS), adult salivary glands (aSG), and male genitalia. These defects are phenocopied by the juvenile hormone mimic methoprene. Four BRC isoforms are produced by alternative splicing of a protein-binding BTB/POZ-encoding exon (BTBBRC) to one of four tandemly duplicated, DNA-binding zinc-finger-encoding exons (Z1BRC, Z2BRC, Z3BRC, Z4BRC). Highly conserved orthologs of BTBBRC and all four ZBRC were found among published cDNA sequences or genome databases from Diptera, Lepidoptera, Hymenoptera, and Coleoptera, indicating that BRC arose and underwent internal exon duplication before the split of holometabolous orders. Tramtrack subfamily members, abrupt, tramtrack, fruitless, longitudinals lacking (lola), and CG31666 were characterized throughout Holometabola and used to root phylogenetic analyses of ZBRC exons, which revealed that the ZBRC clade includes Zabrupt. All four ZBRC domains, including Z4BRC, which has no known essential function, are evolving in a manner consistent with selective constraint. We used transgenic rescue to explore how different BRC isoforms contribute to shared tissue-morphogenesis functions. As predicted from earlier studies, the common CNS and aSG phenotypes were rescued by BRC-Z1 in rbp mutants, BRC-Z2 in br mutants, and BRC-Z3 in 2Bc mutants. However, the isoforms are required at two different developmental stages, with BRC-Z2 and -Z3 required earlier than BRC-Z1. The sequential action of BRC isoforms indicates subfunctionalization of duplicated ZBRC exons even when they contribute to common developmental processes.

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Broad‐Complex function during oogenesis in Drosophila melanogaster

Cited by 14 publications

References 43 publications

Enhancer-trap targeting at the Broad-Complex locus of Drosophila melanogaster.

Enhancer-trap targeting at the Broad-Complex locus of Drosophila melanogaster.

Vitellogenesis and Post-Vitellogenic Maturation of the Insect Ovarian Follicle

Anciently duplicated Broad Complex exons have distinct temporal functions during tissue morphogenesis

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