The Broad-Complex (BR-C) is essential for metamorphosis in Drosophila melanogaster. This locus is coextensive with the 2B5 ecdysone-responsive early puff and is necessary for puffing and transcription of many subsequently activated late genes in the developing salivary gland. Mapping of 31 cDNA clones indicates that approximately 100 kb of the genome is devoted to the synthesis of many BR-C RNAs. Sequence analyses of these cDNA clones show that the BR-C encodes a family of related proteins characterized by a common core amino-terminal domain fused to alternate carboxy domains each containing a pair of zinc fingers. Most proteins also contain domains rich in distinctive amino acids located between the common core and zinc finger regions. BR-C mutant alleles resulting from chromosomal rearrangements at 2B5 are associated with deletions of 5'-untranslated sequences, separation of the core coding domain from the downstream zinc finger domains, or a P element insertional disruption of a zinc finger coding sequence. We infer that the BR-C directly regulates late gene expression by specifying the synthesis of a family of proteins with DNA binding potential.

https://www.genetics.org/content/genetics/129/2/385.full.pdf

The Drosophila Broad-Complex encodes a family of related proteins containing zinc fingers.

The apterous (ap) gene is required for the normal development of the wing and haltere imaginal discs in Drosophila melanogaster. ap encodes a new member of the LIM family of developmental regulatory genes. The deduced amino acid sequence of ap predicts a homeo domain and a cysteine/histidine-rich domain known as the LIM domain. In these domains ap is highly similar to the mec-3 and lin-11 proteins of Caenorhabditis elegans and to the vertebrate insulin enhancer-binding protein isl-1. ap is presumably required for transcriptional regulation of genes involved in wing and haltere development. The nature of the defects in homozygous null mutant flies is consistent with the pattern of ap expression in the larval imaginal discs, ap is also expressed in a complex pattern in the embryo, including portions of the peripheral nervous system (PNS) and central nervous system (CNS). A requirement for ap expression in the larval and adult CNS may be the underlying cause of the defects in hormone production and vitellogenesis described for ap mutations.

/pdf/apterous-a-gene-required-for-imaginal-disc-development-in-40nn9s7i4l.pdf

apterous, a gene required for imaginal disc development in Drosophila encodes a member of the LIM family of developmental regulatory proteins.

The understanding of the molecular basis of the endocrine control of insect metamorphosis has been hampered by the profound differences in responses of the Lepidoptera and the Diptera to juvenile hormone (JH). In both Manduca and Drosophila, the broad (br) gene is expressed in the epidermis during the formation of the pupa, but not during adult differentiation. Misexpression of BR-Z1 during either a larval or an adult molt of Drosophila suppressed stage-specific cuticle genes and activated pupal cuticle genes, showing that br is a major specifier of the pupal stage. Treatment with a JH mimic at the onset of the adult molt causes br re-expression and the formation of a second pupal cuticle in Manduca, but only in the abdomen of Drosophila. Expression of the BR isoforms during adult development of Drosophila suppressed bristle and hair formation when induced early or redirected cuticle production toward the pupal program when induced late. Expression of BR-Z1 at both of these times mimicked the effect of JH application but, unlike JH, it caused production of a new pupal cuticle on the head and thorax as well as on the abdomen. Consequently, the 'status quo' action of JH on the pupal-adult transformation is mediated by the JH-induced re-expression of BR.

Broad specifies pupal development and mediates the ‘status quo’ action of juvenile hormone on the pupal-adult transformation in Drosophila and Manduca

On the basis of the hypothesis that mutants in genes controlling essential cell cycle functions in Drosophila should survive up to the larval-pupal transition, 59 such 'late lethals' were screened for those mutants affecting cell division. Examination of mitosis in brain neuroblasts revealed that 30 of these lethals cause disruptions in mitotic chromosome behavior. These mutants identify genes whose wild-type functions are important for: (1) progression through different steps of interphase, (2) the maintenance of mitotic chromosome integrity, (3) chromosome condensation, (4) spindle formation and/or function, and (5) completion of cytokinesis or completion of chromosome segregation. The presence of mitotic defects in late lethal mutants is correlated tightly with the presence of defective imaginal discs. Thus, the phenotypes of late lethality and poorly developed imaginal discs are together almost diagnostic of mutations in essential cell-cycle functions. The terminal phenotypes exhibited by these Drosophila mitotic mutants are remarkably similar to those observed in mammalian cell-cycle mutants, suggesting that these diverse organisms use a common genetic logic to regulate and integrate the events of the cell cycle.

/pdf/genes-controlling-essential-cell-cycle-functions-in-3vo22hln7p.pdf

Genes controlling essential cell-cycle functions in Drosophila melanogaster.

Krüppel homolog 1 (Kr-h1) mediates juvenile hormone action during metamorphosis of Drosophila melanogaster.

THE metamorphosis of insects provides a model system for the study of hormone action. In Drosophila, metamorphosis is initiated by the formation of a puparium with a rigid cuticle that becomes tanned early in the prepupal period. Subsequently many larval tissues degenerate and the imaginal tissues develop to produce the adult insect. These processes are initiated in Drosophila by the steroid moulting hormone, β-ecdysone1. We are interested in the mechanisms by which β-ecdysone elicits adult development. The recovery of mutants which cannot respond to the hormone would facilitate investigation into the nature of the action of β-ecdysone. We have isolated systematically a series of late larval and prepupal X-linked lethals (ref. 2 and unpublished results of I.K. et al.), about 15% of which are non-pupariating (npr) lethals in which metamorphosis is not initiated. We have investigated whether the npr condition is a result of the autonomous inability of the mutant target tissues to respond normally to β-ecdysone or rather is a stage-specific failure in the production of the hormone. Our results indicate that in most npr lethals the tissue cannot respond to the hormone. Futhermore, we estimate that there are 100–200 such lethals in the genome of D. melanogaster.

Prepupal larval mosaics in Drosophila melanogaster

Twenty-seven late larval or early pupal lethal mutations were isolated for the X-chromosome, some of which showed structural and/or functional deficiencies of the imaginal discs. The mutants were grouped according to the size and morphology of their discs as follows: 1. discs normal: 18 mutants. 2. discs small: 2 mutants. 3. discs degenerate: 4 mutants. 4. discless: 1 mutant. 5. discs heterogeneous: 2 mutants. Preliminary characterization of the mutants included a study of disc morphology, puparium formation and pupal molt, in vivo and in vitro evagination of the imaginal discs, autonomy of the mutation in the disc tissue (differentiation after transplantation and gynander mosaicism test). Possible relations between disc morphology and the former characteristics are discussed.

Isolation and characterization of X-linked lethal mutants affecting differentiation of the imaginal discs in Drosophila melanogaster

A single X-chromosome balancer-bearingCelegans ♂+, as a founder of a strain (AF1), was isolated directly from Fl progeny of irradiated+dpy-8unc-3/lon-2++ hermaphrodites on the basis of the absence of recombinant F2 categories. The balancer chromosome (Bal-X-1) suppresses recombination over a two-thirds section of the X chromosome (between genesdpy-8 andlet-2) and is associated with a reciprocal translocation between linkage groups (LG) X and I. Animals homozygous for the translocation (szT1(X:1)) are nonviable. Hermaphrodites heterozygous for the translocation segregate male selfprogeny at a frequency of 0.08-0.12.Bal-X-l carries the marker mutationlon-2(e678) and can be detected cytologically. This balancer chromosome proved useful for rnaimaininga number of X-linked lethal mutations and deficiencies inC. elegans.

The isolation and genetic analysis of aCaenorhabditis elegants translocation (szT1) strain bearing an X-chromosome balancer

Structure-optimization studies of C-5-C-8-substituted precocene (P) analogues revealed that 1) compounds disubstituted asymmetrically at C-6, C-7 had an anti-allatal effect only if the C-6 side-group was shorter than that at C-7, 2) in the case of C-5, C-7 disubstitution, activity was enhanced by Me at C-5 whereas MeO caused inactivity. Effects of various other substitutions are also discussed.

András Fodor

Papers

Prepupal larval mosaics in Drosophila melanogaster

Isolation and characterization of X-linked lethal mutants affecting differentiation of the imaginal discs in Drosophila melanogaster

The isolation and genetic analysis of aCaenorhabditis elegants translocation (szT1) strain bearing an X-chromosome balancer

Biological activity of precocene analogues on Locusta migratoria

Competition between juvenile hormone antagonist precocene II and juvenile hormone analog: Methoprene in the nematode Caenorhabditis elegans