Food Level in Relation to Rate of Development and Eye Pigmentation in Drosophila Melanogaster

Beadle, G. W.; Tatum, E. L.; Clancy, C. W.

doi:10.2307/1537573

Cited by 173 publications

(150 citation statements)

References 9 publications

(8 reference statements)

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“…As in other animals, growth is affected by feeding, which in Drosophila occurs during the first two and most of the third larval instar. Early in the third instar, larvae reach what is known as critical weight, a point at which holometabolous insects commit to metamorphosis and can develop without further feeding (Beadle et al 1938;Davidowitz et al 2003). Two neuroendocrine pathways have been implicated in coordinating feeding with Drosophila development and overall growth, but our results argue against obvious roles for NF1 in either one.…”

Section: Discussionmentioning

confidence: 61%

Reduced growth of Drosophila neurofibromatosis 1 mutants reflects a non-cell-autonomous requirement for GTPase-Activating Protein activity in larval neurons

Walker¹,

Tchoudakova²,

McKenney³

et al. 2006

Genes Dev.

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Neurofibromatosis type 1 (NF1) is among the most common genetic disorders of humans and is caused by loss of neurofibromin, a large and highly conserved protein whose only known function is to serve as a GTPase-Activating Protein (GAP) for Ras. However, most Drosophila NF1 mutant phenotypes, including an overall growth deficiency, are not readily modified by manipulating Ras signaling strength, but are rescued by increasing signaling through the cAMP-dependent protein kinase A pathway. This has led to suggestions that NF1 has distinct Ras-and cAMP-related functions. Here we report that the Drosophila NF1 growth defect reflects a non-cell-autonomous requirement for NF1 in larval neurons that express the R-Ras ortholog Ras2, that NF1 is a GAP for Ras1 and Ras2, and that a functional NF1-GAP catalytic domain is both necessary and sufficient for rescue. Moreover, a Drosophila p120RasGAP ortholog, when expressed in the appropriate cells, can substitute for NF1 in growth regulation. Our results show that loss of NF1 can give rise to non-cell-autonomous developmental defects, implicate aberrant Ras-mediated signaling in larval neurons as the primary cause of the NF1 growth deficiency, and argue against the notion that neurofibromin has separable Ras-and cAMP-related functions.[Keywords: Neurofibromatosis type 1; organismal growth control; non-cell autonomy; Ras signal transduction; Drosophila melanogaster]Supplemental material is available at http://www.genesdev.org. Neurofibromatosis type 1 (NF1, OMIM 162200) is a common genetic disorder, affecting two to three per 10,000 live births worldwide (Huson and Hughes 1994). NF1 patients are predisposed toward developing a variety of defects, the most characteristic of which include areas of abnormal skin pigmentation and benign tumors associated with peripheral nerves, termed neurofibromas. Less universal but more serious symptoms also include malignant peripheral nerve sheath tumors, other malignancies, and learning disabilities. Developmental abnormalities, such as specific skeletal defects, macrocephaly, and short stature, are also associated with NF1 (Huson and Hughes 1994). The >2800-amino-acid NF1 protein, termed neurofibromin, includes a segment related to the catalytic domains of Ras-specific GTPase-Activating Proteins (GAPs), and ample evidence supports the notion that the ability of neurofibromin to inactivate Ras plays a critical role in the development of NF1-associated tumors (Cichowski and Jacks 2001). The GAP-related domain (GRD) constitutes only ∼15% of neurofibromin, however, and it is less clear whether Ras signaling defects are also the immediate cause of other disease symptoms.A Drosophila melanogaster NF1 ortholog predicts a protein that is ∼60% identical to human neurofibromin over its entire length. We previously reported that Drosophila NF1-null mutants are viable, fertile, and normally patterned, but display a 15%-20% reduction in linear dimensions during all stages of post-embryonic

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Section: Discussionmentioning

confidence: 61%

Reduced growth of Drosophila neurofibromatosis 1 mutants reflects a non-cell-autonomous requirement for GTPase-Activating Protein activity in larval neurons

Walker¹,

Tchoudakova²,

McKenney³

et al. 2006

Genes Dev.

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“…Larvae that are malnourished or insulin-suppressed early in development initiate metamorphosis at the same size as well-fed larvae: (14,39) food deprivation simply slows their growth and delays when they reach critical size. In M. sexta, however, critical size is a function of larval size at the transition to the final larval instar, (12,38) and is influenced by nutrition.…”

Section: Nutrition and Critical Size (B Cs )mentioning

confidence: 99%

Size and shape: the developmental regulation of static allometry in insects

et al. 2007

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SummaryAmong all organisms, the size of each body part or organ scales with overall body size, a phenomenon called allometry. The study of shape and form has attracted enormous interest from biologists, but the genetic, developmental and physiological mechanisms that control allometry and the proportional growth of parts have remained elusive. Recent progress in our understanding of body-size regulation provides a new synthetic framework for thinking about the mechanisms and the evolution of allometric scaling. In particular, insulin/IGF signaling, which plays major roles in longevity, diabetes and the regulation of cell, organ and body size, might also be centrally involved in regulating organismal shape. Here we review recent advances in the fields of growth regulation and endocrinology and use them to construct a developmental model of static allometry expression in insects. This model serves as the foundation for a research program that will result in a deeper understanding of the relationship between growth and form, a question that has fascinated biologists for centuries.

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“…There is a major influence of larval nutrition on adult physiology, as illustrated by the observations of Beadle and colleagues (3). Starving larvae before 70 h AEL results in larval death, whereas starving them after this time point (the "70-h change") results in viable but small adults (3).…”

Section: Larval Nutrition and Adult Physiologymentioning

confidence: 99%

Purine and folate metabolism as a potential target of sex-specific nutrient allocation in Drosophila and its implication for lifespan-reproduction tradeoff

Katzenberger

Hamm

Bonaus

et al. 2006

Physiological Genomics

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. Purine and folate metabolism as a potential target of sex-specific nutrient allocation in Drosophila and its implication for lifespan-reproduction tradeoff. Physiol Genomics 25: 393-404, 2006. First published March 28, 2006 doi:10.1152/physiolgenomics.00009.2006.-The reallocation of metabolic resources is important for survival during periods of limited nutrient intake. This has an influence on diverse physiological processes, including reproduction, repair, and aging. One important aspect of resource allocation is the difference between males and females in response to nutrient stress. We identified several groups of genes that are regulated in a sex-biased manner under complete or protein starvation. These range from expected differences in genes involved in reproductive physiology to those involved in amino acid utilization, sensory perception, immune response, and growth control. A striking difference was observed in purine and the tightly interconnected folate metabolism upon protein starvation. From these results, we conclude that the purine and folate metabolic pathway is a major point of transcriptional regulation during resource allocation and may have relevance for understanding the physiological basis for the observed tradeoff between reproduction and longevity. longevity; microarray analysis; starvation; larval development; metabolic adaptation

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Food Level in Relation to Rate of Development and Eye Pigmentation in Drosophila Melanogaster

Cited by 173 publications

References 9 publications

Reduced growth of Drosophila neurofibromatosis 1 mutants reflects a non-cell-autonomous requirement for GTPase-Activating Protein activity in larval neurons

Reduced growth of Drosophila neurofibromatosis 1 mutants reflects a non-cell-autonomous requirement for GTPase-Activating Protein activity in larval neurons

Size and shape: the developmental regulation of static allometry in insects

Purine and folate metabolism as a potential target of sex-specific nutrient allocation in Drosophila and its implication for lifespan-reproduction tradeoff

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