Heat shock and Phenocopy induction in Drosophila

Mitchell, Herschel K.; Lipps, Loveriza S.

doi:10.1016/0092-8674(78)90275-1

Cited by 108 publications

(47 citation statements)

References 19 publications

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“…Other Drosophila phenocopies such as multiple wing hair reflect closer spacing of heat shock sensitivity and phenotype; here, heat shock at different specific times through the pupal stage yields multiple hairs on different parts of the adult fly (Mitchell and Lipps, 1978;Petersen and Mitchell, 1987). Phenocopies are not restricted to Drosophila; similar developmental interference by heat shock has been reported in Xenopus and in mammalian embryogenesis (Elsdale, Pearson, and Whitehead, 1976;Witting et al, 1983).…”

Section: Heat Shock Arrests the Development Of Globular Embryosmentioning

confidence: 70%

Novel regulation of heat shock genes during carrot somatic embryo development.

et al. 1989

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We have determined that somatic embryos of carrot exhlbit a number of lnterestlng and unusual propertles when exposed to heat shock at different times in thelr development. Speclflcally, we have seen that mld-globular embryos can be arrested lrreversibly in thelr development when heat-shocked, whereas all other stages of embryogenesls, both before and after this stage, are fully capable of normal development after the stress. In lnvestlgatlng the molecular basis of this developmental sensltivity to heat shock, uslng a cloned heat shock gene encodlng a small heat shock protein, we have determined that globular embryos both synthesire and accumulate slgnlflcantly less heat shock mRNA when compared with embryO8 of any other stage or to callus suspension cells. In fact, there appears to be no transcriptional induction of heat shock gene expression in response to heat shock during this time period; the gene i8 expressed at the same relatively low Ievel both before and after heat shock. However, in spite of the low level of heat shock mRNA available, globular embryos synthesire the full complement of heat shock proteins in response to heat treatment. l h e globular embryos appear to accomplish this by translating the existing heat shock mRNAs at an elevated rate, which compensates for the low level of available mRNA. Once the embryos have progressed beyond the globular stage of development, regulation at the transcriptional level resumes, and the embryos again exhibit normal development after heat shock.

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Section: Heat Shock Arrests the Development Of Globular Embryosmentioning

confidence: 70%

Novel regulation of heat shock genes during carrot somatic embryo development.

et al. 1989

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“…The HSP also play a role in development, as shown most clearly in Drosophila melanogaster by Mitchell and associates (24,29). In the absence of stress, HSP appear at precisely timed points during the flies' developmental cycle.…”

Section: Discussionmentioning

confidence: 95%

Mammalian stress proteins HSP70 and HSP28 coinduced by nicotine and either ethanol or heat.

Hahn¹,

Shiu²,

Auger³

1991

Mol. Cell. Biol.

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Cells exposed to a variety of stresses such as heat or ethanol respond by increasing their rate of synthesis of a set of proteins termed heat shock proteins (HSP). These proteins then appear to offer protection against the stressor and many other insults. The HSP also play important roles in unstressed cells. They are involved in the regulation of the cell cycle and during specific stages in the development of organisms. Exposure to stress during development (e.g., in pupal stages of insects or during gestation in mammals) leads to birth defects that are specific to the timing of the stress. It has been hypothesized that the ill-timed induction of HSP is responsible for this phenomenon. Epidemiological studies in humans have related teratogenic events to maternal exposures to hyperthermia or ethanol during pregnancy. The rate of alcohol-induced birth defects is greatly enhanced by smoking, suggesting a role for nicotine. Nicotine by itself, however, is said not to induce HSP. We hypothesized that nicotine may act as a coinducer (or facilitator) of stress responses. This possibility we tested on three levels: protection against heat (thermotolerance), induction of specific HSP, and binding of the heat shock transcription factor to the heat shock element. Each of these tests showed clearly that nicotine does indeed play such a role. This places nicotine in a novel position; to date, no other coinducers of stress responses have been reported. Our results may offer an explanation for the epidemiological data cited earlier.Stress responses in mammalian cells are characterized by two readily measured events. First, the protein synthesis pattern of the stressed cell is modified. The rates of synthesis of many normal cell proteins are reduced, while the synthesis of a specific set of proteins (and the relevant mRNAs) is either enhanced or induced de novo. These latter proteins are termed stress proteins and are of two types: proteins common to many stresses and proteins specific to the individual inducer (23). The second event is the development, in the surviving cells, of a transient resistance to the stressor; this is frequently accompanied by cross-resistance to other inducers (10, 13, 21). Many investigators have suggested that the stress proteins are responsible for this induced resistance, although direct proof is lacking (20,36).Among the inducers of stress responses are heat shock; exposure to aliphatic alcohols (including ethanol), metals such as cadmium, or sodium arsenite; and release of cells from hypoxia (23). A common feature of these treatments is protein damage. Indeed, several studies have shown that damaged proteins or the intracellular presence of proteins deemed "foreign" by the cell can lead to the induction of a response that is similar to that seen after heat shock (1, 14, 19). The heat shock response has been studied far more extensively than any other stress response. The reasons for this include the current interest in the use of hyperthermia in cancer therapy, the ease of induction of the resp...

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“…1.3). A possible reason for this effect is that temperature shock freezes the progression of pattern determination, possibly by activating heat shock or stress proteins that stop biosynthetic or transcriptional activity (Mitchell and Lipps 1978;Crews et al 2016;Welte et al 1995). The grassfire model shows that a single pattern element can split into two and that both ocelli and parafocal elements can be produced from a common source.…”

Section: Fusion and Separation Of Ocelli And Parafocal Elementsmentioning

confidence: 99%

The Common Developmental Origin of Eyespots and Parafocal Elements and a New Model Mechanism for Color Pattern Formation

Nijhout

2017

Diversity and Evolution of Butterfly Wing Patterns

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The border ocelli and adjacent parafocal elements are among the most diverse and finely detailed features of butterfly wing patterns. The border ocelli can be circular, elliptical, and heart-shaped or can develop as dots, arcs, or short lines. Parafocal elements are typically shaped like smooth arcs but are also often "V," "W," and "M" shaped. The fusion of a border ocellus with its adjacent parafocal element is a common response to temperature shock and treatment with chemicals such as heparin and tungstate ions. Here I develop a new mathematical model for the formation of border ocelli and parafocal elements. The models are a reactiondiffusion model based on the well-established gradient-threshold mechanisms in embryonic development. The model uses a simple biochemical reaction sequence that is initiated at the wing veins and from there spreads across the field in the manner of a grass-fire. Unlike Turing-style models, this model is insensitive to the size of the field. Like real developmental systems, the model does not have a steady state, but the pattern is "read out" at a point in development, in response to an independent developmental signal such as a pulse of ecdysone secretion, which is known to regulate color pattern in butterflies. The grass-fire model reproduces the sequence of Distal-less expression that determines the position of eyespot foci and also shows how a border ocellus and its neighboring parafocal element can arise from such a single focus. The grass-fire model shows that the apparent fusion of ocellus and parafocal element is probably due to a premature termination of the normal process that separates the two and supports the hypothesis that the parafocal element is the distal band of the border symmetry system.

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Heat shock and Phenocopy induction in Drosophila

Cited by 108 publications

References 19 publications

Novel regulation of heat shock genes during carrot somatic embryo development.

Novel regulation of heat shock genes during carrot somatic embryo development.

Mammalian stress proteins HSP70 and HSP28 coinduced by nicotine and either ethanol or heat.

The Common Developmental Origin of Eyespots and Parafocal Elements and a New Model Mechanism for Color Pattern Formation

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