Plastic flies

Shingleton, Alexander W.; Tang, Hui

doi:10.4161/fly.20323

Cited by 22 publications

(10 citation statements)

References 49 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Second, developmental genetic manipulations alter the slope of trait–body scaling in D. melanogaster (e.g., Tang et al. 2011; Shingleton and Tang 2012), suggesting slope evolution could occur among taxa through these evolutionarily conserved genetic pathways. Finally, the slopes of scaling relationships evolve among species over the longer term (e.g., Burkhardt and de la Motte 1985; Baker and Wilkinson 2001; Emlen et al.…”

Section: Discussionmentioning

confidence: 99%

“…2011; Emlen et al. 2012; Shingleton and Tang 2012; Warren et al. 2013), and therefore may be less likely or unable to contribute to slope evolution without also affecting the bivariate mean.…”

Section: Discussionmentioning

confidence: 99%

“…(See reviews in Baker and Wilkinson 2001; Frankino et al. 2009; Shingleton and Tang 2012; Pélabon et al. 2014; Voje et al.…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Individual Cryptic Scaling Relationships and the Evolution of Animal Form

Frankino

Bakota

Dworkin

et al. 2019

Integrative and Comparative Biology

View full text Add to dashboard Cite

Artificial selection offers a powerful tool for the exploration of how selection and development shape the evolution of morphological scaling relationships. An emerging approach models the expression and evolution of morphological scaling relationships as a function of variation among individuals in the developmental mechanisms that regulate trait growth. These models posit the existence of genotype-specific morphological scaling relationships that are unseen or “cryptic.” Within-population allelic variation at growth-regulating loci determines how these individual cryptic scaling relationships are distributed, and exposure to environmental factors that affect growth determines the size phenotype expressed by each individual on their cryptic, genotype-specific scaling relationship. These models reveal that evolution of the intercept and slope of the population-level static allometry is determined, often in counterintuitive ways, largely by the shape of the distribution of these underlying individual-level scaling relationships. Here we review this modeling framework and present the wing-body size individual cryptic scaling relationships from a population of Drosophila melanogaster. To determine how these models might inform interpretation of published work on scaling relationship evolution, we review studies where artificial selection was applied to alter the parameters of population-level static allometries. Finally, motivated by our review, we outline areas in need of empirical work and describe a research program to address these topics; the approach includes describing the distribution of individual cryptic scaling relationships across populations and environments, empirical testing of the model’s predictions, and determining the effects of environmental heterogeneity on realized trait distributions and how this affects allometry evolution.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Individual Cryptic Scaling Relationships and the Evolution of Animal Form

Frankino

Bakota

Dworkin

et al. 2019

Integrative and Comparative Biology

View full text Add to dashboard Cite

show abstract

“…Changing the level of activity of IIS/TOR appears to be a common mechanism for regulating the degree of plasticity in organ size. In Drosophila , changes in the expression of either FoxO or InR generate disproportionate growth of the wing in relation to body size (Shingleton and Tang, 2012), indicating that modulating IIS/TOR signaling at several levels of its action can produce exaggerated organ growth (Shingleton and Frankino, 2012; Shingleton and Tang, 2012). …”

Section: Tissue-specific Sensitivities To Iis/tor Signalingmentioning

confidence: 99%

Mechanisms regulating nutrition-dependent developmental plasticity through organ-specific effects in insects

Kaburagi¹,

Mendes²,

Mirth³

2013

Front. Physiol.

112

View full text Add to dashboard Cite

Nutrition, via the insulin/insulin-like growth factor (IIS)/Target of Rapamycin (TOR) signaling pathway, can provide a strong molding force for determining animal size and shape. For instance, nutrition induces a disproportionate increase in the size of male horns in dung and rhinoceros beetles, or mandibles in staghorn or horned flour beetles, relative to body size. In these species, well-fed male larvae produce adults with greatly enlarged horns or mandibles, whereas males that are starved or poorly fed as larvae bear much more modest appendages. Changes in IIS/TOR signaling plays a key role in appendage development by regulating growth in the horn and mandible primordia. In contrast, changes in the IIS/TOR pathway produce minimal effects on the size of other adult structures, such as the male genitalia in fruit flies and dung beetles. The horn, mandible and genitalia illustrate that although all tissues are exposed to the same hormonal environment within the larval body, the extent to which insulin can induce growth is organ specific. In addition, the IIS/TOR pathway affects body size and shape by controlling production of metamorphic hormones important for regulating developmental timing, like the steroid molting hormone ecdysone and sesquiterpenoid hormone juvenile hormone. In this review, we discuss recent results from Drosophila and other insects that highlight mechanisms allowing tissues to differ in their sensitivity to IIS/TOR and the potential consequences of these differences on body size and shape.

show abstract

“…Although the proximate mechanisms that stabilize size in the imaginal discs are still unclear, one firm candidate is the transcription factor FOXO [163]. The transcription factor FOXO negatively modulates tissue growth and is a central hub of multiple signalling pathways that regulate cell growth, differentiation, and survival including the insulin/IGF signalling pathway, the JH and ecdysone signalling in response to many perturbations and in the protection against stress stimuli [35, 164, 165] and these characteristics make FOXO a candidate of size and symmetry regulation in the imaginal discs. Indeed, systemic activation of Dilp8 in the absence of perturbations triggers the developmental checkpoint and slows down the compensatory growth response associated with regulation of FOXO activity in imaginal discs [14, 16].…”

Section: Sensing Perturbations Damage and Fitness In Growing Organsmentioning

confidence: 99%

Systemic signalling and local effectors in developmental stability, body symmetry, and size

Juarez-Carreño¹,

Morante²,

Domı́nguez³

2018

CST

View full text Add to dashboard Cite

Symmetric growth and the origins of fluctuating asymmetry are unresolved phenomena of biology. Small, and sometimes noticeable, deviations from perfect bilateral symmetry reflect the vulnerability of development to perturbations. The degree of asymmetry is related to the magnitude of the perturbations and the ability of an individual to cope with them. As the left and right sides of an individual were presumed to be genetically identical, deviations of symmetry were traditionally attributed to non-genetic effects such as environmental and developmental noise. In this review, we draw attention to other possible sources of variability, especially to somatic mutations and transposons. Mutations are a major source of phenotypic variability and recent genomic data have highlighted somatic mutations as ubiquitous, even in phenotypically normal individuals. We discuss the importance of factors that are responsible for buffering and stabilizing the genome and for maintaining size robustness and quality through elimination of less-fit or damaged cells. However, the important question that arises from these studies is whether this self-correcting capacity and intrinsic organ size controls are sufficient to explain how symmetric structures can reach an identical size and shape. Indeed, recent discoveries in the fruit fly have uncovered a conserved hormone of the insulin/IGF/relaxin family, Dilp8, that is responsible for stabilizing body size and symmetry in the face of growth perturbations. Dilp8 alarm signals periphery growth status to the brain, where it acts on its receptor Lgr3. Loss of Dilp8-Lgr3 signaling renders flies incapable of detecting growth perturbations and thus maintaining a stable size and symmetry. These findings help to understand how size and symmetry of somatic tissues remain undeterred in noisy environments, after injury or illnesses, and in the presence of accumulated somatic mutations.

show abstract

Plastic flies

Cited by 22 publications

References 49 publications

Individual Cryptic Scaling Relationships and the Evolution of Animal Form

Individual Cryptic Scaling Relationships and the Evolution of Animal Form

Mechanisms regulating nutrition-dependent developmental plasticity through organ-specific effects in insects

Systemic signalling and local effectors in developmental stability, body symmetry, and size

Contact Info

Product

Resources

About