Two Drosophila Regulatory Genes, Deformed and the Broad-Complex, Share Common Functions in Development of Adult CNS, Head, and Salivary Glands

Restifo, Linda L.; Merrill, V. K. L.

doi:10.1006/dbio.1994.1102

Cited by 28 publications

(20 citation statements)

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“…Prepupae and pupae were aged at 25°C under highhumidity conditions as previously described (Restifo and White, 1991). We found these high-humidity conditions and the corn flour-based larval culture medium (see above) ideal for maximizing the maturational potential of developmental mutants (Restifo and White, 1991;Restifo and Merrill, 1994). A "pharate adult" stage (P14 -15), within hours of adult emergence, was chosen for most analyses because brain development has reached mature adult morphology, and the lack of muscle activity and lack of air in the tracheal system allow for optimal dissection and fixation (Restifo and White, 1991).…”

Section: Methodsmentioning

confidence: 98%

Defective Neuronal Development in the Mushroom Bodies ofDrosophila Fragile X Mental Retardation 1Mutants

Michel¹,

Kraft²,

Restifo³

2004

J. Neurosci.

140

149

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Fragile X mental retardation 1 (Fmr1) is a highly conserved gene with major roles in CNS structure and function. Its product, the RNA-binding protein FMRP, is believed to regulate translation of specific transcripts at postsynaptic sites in an activity-dependent manner. Hence, Fmr1 is central to the molecular mechanisms of synaptic plasticity required for normal neuronal maturation and cognitive ability. Mutations in its Drosophila ortholog, dfmr1, produce phenotypes of brain interneurons and axon terminals at the neuromuscular junction, as well as behavioral defects of circadian rhythms and courtship. We hypothesized that dfmr1 mutations would disrupt morphology of the mushroom bodies (MBs), highly plastic brain regions essential for many forms of learning and memory. We found developmental defects of MB lobe morphogenesis, of which the most common is a failure of ␤ lobes to stop at the brain midline. A similar recessive ␤-lobe midline-crossing phenotype has been previously reported in the memory mutant linotte. The dfmr1 MB defects are highly sensitive to genetic background, which is reminiscent of mammalian fragile-X phenotypes. Mutations of dfmr1 also interact with one or more third-chromosome loci to promote ␣/␤-lobe maturation. These data further support the use of the Drosophila model system for study of hereditary cognitive disorders of humans.

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Section: Methodsmentioning

confidence: 98%

Defective Neuronal Development in the Mushroom Bodies ofDrosophila Fragile X Mental Retardation 1Mutants

Michel¹,

Kraft²,

Restifo³

2004

J. Neurosci.

140

149

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“…Stocks: BR-C mutant alleles used in this study were previously used to investigate internal tissue metamorphosis White 1991, 1992;Restifo and Merrill 1994;Sandstrom et al 1997;Consoulas et al 2005). BR-C mutant progeny were identified by visible markers yellow, white, and/or singed.…”

Section: Methodsmentioning

confidence: 99%

Interaction Between Hormonal Signaling Pathways in Drosophila melanogaster as Revealed by Genetic Interaction Between Methoprene-tolerant and Broad-Complex

et al. 2006

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Juvenile hormone ( JH) regulates insect development by a poorly understood mechanism. Application of JH agonist insecticides to Drosophila melanogaster during the ecdysone-driven onset of metamorphosis results in lethality and specific morphogenetic defects, some of which resemble those in mutants of the ecdysone-regulated Broad-Complex (BR-C). The Methoprene-tolerant (Met) bHLH-PAS gene mediates JH action, and Met mutations protect against the lethality and defects. To explore relationships among these two genes and JH, double mutants were constructed between Met alleles and alleles of each of the BR-C complementation groups: broad (br), reduced bristles on palpus (rbp), and 2Bc. Defects in viability and oogenesis were consistently more severe in rbp Met or br Met double mutants than would be expected if these genes act independently. Additionally, complementation between BR-C mutant alleles often failed when MET was absent. Patterns of BRC protein accumulation during metamorphosis revealed essentially no difference between wild-type and Met-null individuals. JH agonist treatment did not block accumulation of BRC proteins. We propose that MET and BRC interact to control transcription of one or more downstream effector genes, which can be disrupted either by mutations in Met or BR-C or by application of JH/JH agonist, which alters MET interaction with BRC.

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“…The Methoprene-tolerant (Met) alleles tested were ethyl methanesulfonate induced [Wilson and Fabian, 1987] in either an Ore-RC genetic background (Met 1 ) [Wilson and Fabian, 1986] or a yellow vermilion background (Met 3 ) . Also examined were 2Bc 2 , a recessive BRC mutation causing early-midpupal lethality [Belyaeva et al, 1980;White, 1991, 1992], and Deformed rV8 , a recessive viable allele that causes late-pupal lethality when hemizygous, e.g., in combination with Df(3R)Scr [Merrill et al, 1987;Restifo and Merrill, 1994]. Chromosomal markers [Lindsley and Zimm, 1992] are given in the figure legends.…”

Section: Stocksmentioning

confidence: 99%

A juvenile hormone agonist reveals distinct developmental pathways mediated by Ecdysone-inducible broad complex transcription factors

Restifo

Wilson

1998

Dev. Genet.

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Two Drosophila Regulatory Genes, Deformed and the Broad-Complex, Share Common Functions in Development of Adult CNS, Head, and Salivary Glands

Cited by 28 publications

References 0 publications

Defective Neuronal Development in the Mushroom Bodies ofDrosophila Fragile X Mental Retardation 1Mutants

Defective Neuronal Development in the Mushroom Bodies ofDrosophila Fragile X Mental Retardation 1Mutants

Interaction Between Hormonal Signaling Pathways in Drosophila melanogaster as Revealed by Genetic Interaction Between Methoprene-tolerant and Broad-Complex

A juvenile hormone agonist reveals distinct developmental pathways mediated by Ecdysone-inducible broad complex transcription factors

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