Regulation of white locus expression: The structure of mutant alleles at the white locus of Drosophila melanogaster

Zachar, Zuzana; Bingham, Paul M.

doi:10.1016/0092-8674(82)90250-1

Cited by 165 publications

(100 citation statements)

References 28 publications

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“…To rule out the possibility that cell death affects w expression as the basis of the above results, we crossed Dr or B to hypomorphic w mutants including point mutations w a2 and w a3 and insertion mutations, w-blood (w bl ) and w-apricot (w a ) (Zachar and Bingham 1982) and found no impact (Figure S2). These results indicate that modulation of the white gene itself is not the basis for the suppression.…”

Section: Resultsmentioning

confidence: 99%

Inhibition of RNA Interference and Modulation of Transposable Element Expression by Cell Death in Drosophila

2011

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RNA interference (RNAi) regulates gene expression by sequence-specific destruction of RNA. It acts as a defense mechanism against viruses and represses the expression of transposable elements (TEs) and some endogenous genes. We report that mutations and transgene constructs that condition cell death suppress RNA interference in adjacent cells in Drosophila melanogaster. The reversal of RNAi is effective for both the white (w) eye color gene and green fluorescent protein (GFP), indicating the generality of the inhibition. Antiapoptotic transgenes that reverse cell death will also reverse the inhibition of RNAi. Using GFP and a low level of cell death produced by a heat shock-head involution defective (hs-hid) transgene, the inhibition appears to occur by blocking the conversion of double-stranded RNA (dsRNA) to short interfering RNA (siRNA). We also demonstrate that the mus308 gene and endogenous transposable elements, which are both regularly silenced by RNAi, are increased in expression and accompanied by a reduced level of siRNA, when cell death occurs. The finding that chronic ectopic cell death affects RNAi is critical for an understanding of the application of the technique in basic and applied studies. These results also suggest that developmental perturbations, disease states, or environmental insults that cause ectopic cell death would alter transposon and gene expression patterns in the organism by the inhibition of small RNA silencing processes.

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Section: Resultsmentioning

confidence: 99%

Inhibition of RNA Interference and Modulation of Transposable Element Expression by Cell Death in Drosophila

2011

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“…Additionally, the bw 1 and st 1 mutations were outcrossed to wild-type flies for greater than six generations (Dreesen et al 1988;Tearle et al 1989). The w 1 , w a , w a2 , w a3 , w ec3 , and temperature-sensitive w bl flies were not cantonized (Bingham and Judd 1981;Zachar and Bingham 1982;Bingham and Chapman 1986;Birchler and Hiebert 1989). The outcrossing schemes used at least 20 males and females in each generation.…”

Section: Genetic Manipulations and Culture Conditionsmentioning

confidence: 99%

“…(The w 1 and w a mutations have transposable elements in regulatory regions of the gene [Zachar and Bingham 1982;O'Hare et al 1991]). …”

Section: Learning and Memory 75mentioning

confidence: 99%

Genetic dissociation of acquisition and memory strength in the heat-box spatial learning paradigm in Drosophila

Diegelmann¹,

Zars²,

Zars³

2006

Learn. Mem.

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Memories can have different strengths, largely dependent on the intensity of reinforcers encountered. The relationship between reinforcement and memory strength is evident in asymptotic memory curves, with the level of the asymptote related to the intensity of the reinforcer. Although this is likely a fundamental property of memory formation, relatively little is known of how memory strength is determined. Memory performance at different levels in Drosophila can be measured in an operant heat-box conditioning paradigm. In this spatial learning paradigm, flies learn and remember to avoid one-half of a dark chamber associated with a temperature outside of the preferred range. The reinforcement temperature has a strong effect on the level of learning in wild-type flies, with higher temperatures inducing stronger memories. Additionally, two mutations alter memory-acquisition curves, either changing acquisition rate or asymptotic memory level. The rutabaga mutation, affecting a type-1 adenylyl cyclase, decreases the acquisition rate. In contrast, the white mutation, modifying an ABC transporter, limits asymptotic memory. The white mutation does not negatively affect classical olfactory conditioning but actually improves performance at low reinforcement levels. Thus, memory acquisition/memory strength and classical olfactory/operant spatial memories can be genetically dissociated. A conceptual model of operant conditioning and the levels at which rutabaga and white influence conditioning is proposed.Memories are formed from unexpected experiences. Eventually, a sensory cue or behavior predicts positive or negative consequences. Importantly, memory strength depends on the intensity of those reinforcing stimuli such that weak reinforcers support memories of limited magnitude. This relationship is evident in asymptotic acquisition curves where the asymptote level is related to the intensity of the reinforcer. This has been found in operant and classical conditioning paradigms with both positive and negative reinforcers in many species (Herrnstein 1997), including several species of insects (e.g., in rewarded classical and operant conditioning in the honeybee and negatively associated olfactory classical conditioning in Drosophila) (Menzel and Erber 1972;Bitterman et al. 1983;Tully and Quinn 1985;Loo and Bitterman 1992). The repeated finding of the positive relationship between reinforcement intensity and memory strength indicates that this is a fundamental property of learning.The biogenic amines (e.g., serotonin, dopamine, and octopamine) can function as teaching signals. These are the molecules that, together with sensory-based depolarization, feed into the cAMP/PKA and NMDA-receptor pathways. The biochemical changes in this pathway support synaptic plasticity and memory formation. In the Aplysia model of heterosynaptic plasticity, serotonin mediates the tail shock and is a sufficient teaching signal with in vitro synaptic plasticity tests (Martin et al. 1997;Kandel 2001). Dopamine is also critical in memory formation....

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“…It would have been surprising if no phenotypic effects resulted from the insertion of mobile genetic elements into eukaryotic genes, and indeed many are seen which parallel the observations made in prokaryotes (McLintock, 1956;Green, 1980;Bingham & Judd, 1981;Levis & Rubin, 1982, McGinnis et al, 1983Perlman, 1983). These include examples of non-lethal transposable element insertions into defined genetic loci, both in plants (Johns et al, 1985) and in Drosophila (Zachar & Bingham, 1982) where they may be a significant source of natural mutations. Non-lethal gene insertions which have no severe phenotypic effect can clearly be tolerated.…”

Section: Introductionmentioning

confidence: 73%

Structure and function of repetitive DNA in eukaryotes

Hardman¹

1986

Biochemical Journal

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Regulation of white locus expression: The structure of mutant alleles at the white locus of Drosophila melanogaster

Cited by 165 publications

References 28 publications

Inhibition of RNA Interference and Modulation of Transposable Element Expression by Cell Death in Drosophila

Inhibition of RNA Interference and Modulation of Transposable Element Expression by Cell Death in Drosophila

Genetic dissociation of acquisition and memory strength in the heat-box spatial learning paradigm in Drosophila

Structure and function of repetitive DNA in eukaryotes

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