Isolation and characterization of novel mutations of the Broad-Complex, a key regulatory gene of ecdysone induction in Drosophila melanogaster

Gonzy, G; Pokholkova, Galina V.; Peronnet, Frédérique; Mugat, Bruno; Demakova, Olga V.; Kotlikova, Irina V.; Lepesant, Jean Antoine; Жимулев, И. Ф.

doi:10.1016/s0965-1748(01)00097-2

Cited by 21 publications

(14 citation statements)

References 33 publications

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“…EM double immunostaining reveals that DCC and Po1IIo can map to close but still distinct areas within a single interband: Since the majority of factors involved in transcription localize on polytene chromosomes to the regions of decondensed chromatin, namely to interbands and puffs (Champlin et al 1991;Weeks et al 1993;Stokes et al 1996;Kaplan et al 2000;Gerber et al 2001;Gonzy et al 2002;Saunders et al 2003), it is no wonder that light-microscopy analysis of the DCC and PolIIo patterns on the male X revealed a significant degree of overlap in many regions (except puffs and cytologically extensive DCC gaps). However, we noted a number of regions where distinct MSL-binding sites could be observed, whereas the RNA polymerase was undetectable ( Figure 1).…”

Section: Resultsmentioning

confidence: 99%

The Drosophila Dosage Compensation Complex Binds to Polytene Chromosomes Independently of Developmental Changes in Transcription

et al. 2006

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In Drosophila, the dosage compensation complex (DCC) mediates upregulation of transcription from the single male X chromosome. Despite coating the polytene male X, the DCC pattern looks discontinuous and probably reflects DCC dynamic associations with genes active at a given moment of development in a salivary gland. To test this hypothesis, we compared binding patterns of the DCC and of the elongating form of RNA polymerase II (PolIIo). We found that, unlike PolIIo, the DCC demonstrates a stable banded pattern throughout larval development and escapes binding to a subset of transcriptionally active areas, including developmental puffs. Moreover, these proteins are not completely colocalized at the electron microscopy level. These data combined imply that simple recognition of PolII machinery or of general features of active chromatin is either insufficient or not involved in DCC recruitment to its targets. We propose that DCC-mediated site-specific upregulation of transcription is not the fate of all active X-linked genes in males. Additionally, we found that DCC subunit MLE associates dynamically with developmental and heat-shock-induced puffs and, surprisingly, with those developing within DCC-devoid regions of the male X, thus resembling the PolIIo pattern. These data imply that, independently of other MSL proteins, the RNA-helicase MLE might participate in general transcriptional regulation or RNA processing.

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Section: Resultsmentioning

confidence: 99%

The Drosophila Dosage Compensation Complex Binds to Polytene Chromosomes Independently of Developmental Changes in Transcription

et al. 2006

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“…This suggests that viability was an ancestral function of BRC, rather than a new function acquired after the time of exon duplication; this is true regardless of Z4 functionality. It is likely that BRC-Z4 is not required for viability; multiple genetic screens have been done since npr1 1 (a null allele for all BRC functions) was first described (Stewart et al 1972), and no lethal mutations affecting Z4 structure or expression have been identified (Kiss et al 1976(Kiss et al , 1988Belyaeva et al 1980;DiBello et al 1991;Gonzy et al 2002). Together, the available data suggest that the function of the exon that duplicated to generate Z1 and Z4 was more similar to that of Z1 and that Z4 is the newest exon.…”

Section: Subfunctionalization Of Brc Roles In Tissue Morphogenesismentioning

confidence: 99%

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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“…Here we used dbd to investigate the effects of the Z3 isoform of the BTB/POZ zinc-finger transcription factor Broad (BrZ3) on dendritic development in intact animals. Broad is best known for transducing 20-hydroxyecdysone signals into transcriptional cascades at metamorphosis [15-17]. In D. melanogaster , the four Broad splice variants have unique carboxy-terminal zinc-finger pairs (Z1 to Z4), which serve tissue-specific independent, partially redundant, and combinatorial functions [16].…”

Section: Introductionmentioning

confidence: 99%

The BTB/POZ zinc finger protein Broad-Z3 promotes dendritic outgrowth during metamorphic remodeling of the peripheral stretch receptor dbd

2011

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BackgroundVarious members of the family of BTB/POZ zinc-finger transcription factors influence patterns of dendritic branching. One such member, Broad, is notable because its BrZ3 isoform is widely expressed in Drosophila in immature neurons around the time of arbor outgrowth. We used the metamorphic remodeling of an identified sensory neuron, the dorsal bipolar dendrite sensory neuron (dbd), to examine the effects of BrZ3 expression on the extent and pattern of dendrite growth during metamorphosis.ResultsUsing live imaging of dbd in Drosophila pupae, we followed its normal development during metamorphosis and the effect of ectopic expression of BrZ3 on this development. After migration of its cell body, dbd extends a growth-cone that grows between two muscle bands followed by branching and turning back on itself to form a compact dendritic bundle. The ectopic expression of the BrZ3 isoform, using the GAL4/UAS system, caused dbd's dendritic tree to transform from its normal, compact, fasciculated form into a comb-like arbor that spread over on the body wall. Time-lapse analysis revealed that the expression of BrZ3 caused the premature extension of the primary dendrite onto immature myoblasts, ectopic growth past the muscle target region, and subsequent elaboration onto the epidermis. To control the timing of expression of BrZ3, we used a temperature-sensitive GAL80 mutant. When BrZ3 expression was delayed until after the extension of the primary dendrite, then a normal arbor was formed. By contrast, when BrZ3 expression was confined to only the early outgrowth phase, then ectopic arbors were subsequently formed and maintained on the epidermis despite the subsequent absence of BrZ3.ConclusionsThe adult arbor of dbd is a highly branched arbor whose branches self-fasciculate to form a compact dendritic bundle. The ectopic expression of BrZ3 in this cell causes a premature extension of its growth-cone, resulting in dendrites that extend beyond their normal muscle substrate and onto the epidermis, where they form a comb-shaped, ectopic arbor. Our quantitative data suggest that new ectopic arbor represents an 'unpacking' of the normally fasciculated arbor onto the epidermis. These data suggest that the nature of their local environment can change dendrite behavior from self-adhesion to self-avoidance.

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Isolation and characterization of novel mutations of the Broad-Complex, a key regulatory gene of ecdysone induction in Drosophila melanogaster

Cited by 21 publications

References 33 publications

The Drosophila Dosage Compensation Complex Binds to Polytene Chromosomes Independently of Developmental Changes in Transcription

The Drosophila Dosage Compensation Complex Binds to Polytene Chromosomes Independently of Developmental Changes in Transcription

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

The BTB/POZ zinc finger protein Broad-Z3 promotes dendritic outgrowth during metamorphic remodeling of the peripheral stretch receptor dbd

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