Biology subjects

Shingleton, A. W.

Publications and source records attributed to Shingleton, A. W..

7 recordsLinked to original sources

bioRxiv2026

Room to breathe: Nutrition and developmental oxygen modulate the crowding effect on size in Drosophila melanogaster

In a wide variety of animals, developmental crowding results in adults with smaller bodies. The crowding effect on body size in Drosophila melanogaster is canonically attributed to heightened competition for nutrition. However, whether other consequences of crowding also contribute to its effect on size remains an open question. We tested the relative contributions of nutritional competition, oxygen availability, and larval-generated metabolites to the crowding effect on size. We found that while nutrition explains most of the variation in body size due to crowding, oxygen also contributes in a sex- and nutrition-dependent manner. We found no evidence that larval-generated chemicals affect body size. These data confirm a widely suspected but untested role of nutrition in producing the crowding effect on size in D. melanogaster, while revealing an unexpected role of oxygen, and raise the possibility that behavior may be a mediator of density-dependent plasticity. Research HighlightsWe found that both nutrition and oxygen mediate the crowding effect on size in Drosophila melanogaster.

developmental biology↗

bioRxiv2026

Scaling Across Environments: Temperature and nutrition independently shape the genetics of size plasticity and morphological scaling

Across animals, variation in adult body size is accompanied by coordinated variation in the size of individual morphological traits. However, the same morphological trait can scale differently with body size depending on what drives the size variation. In Drosophila melanogaster, for example, wing size scales differently with body size when size varies because of developmental nutrition versus developmental temperature. Whether the genetic basis of size plasticity and scaling is shared across different environmental regulators of size remains unclear, but is central to predicting how selection acts on the developmental mechanisms that regulate trait size, plasticity and morphological scaling. Using ~200 isogenic D. melanogaster lineages, we measured wing and leg size across nutritional and thermal treatments. For each lineage, we estimated nutritional and thermal plasticity for both traits, as well as the wing-leg individual-level scaling relationship, or ILSR, generated by each environmental source of size variation. We found extensive genetic variation in both thermal and nutritional plasticity for wings and legs, and in the slope of the ILSR between them. However, a lineages thermal plasticity was genetically uncorrelated with its nutritional plasticity for either trait, and we detected no genetic correlation between the slopes of thermal and nutritional wing-leg ILSRs. We also found no genetic correlation in the slope of nutritional wing-leg ILSRs across temperatures. Thus, the slope of a lineages nutritional ILSR at 17{degrees}C was not predictive of its slope at 25{degrees}C of 28{degrees}C. Nevertheless, the overall pattern of nutritional ILSRs was conserved across temperatures. These results suggest that the genetic architecture of size plasticity and scaling depends on the environmental source of size variation. Consequently, the evolutionary response of scaling to selection in heterogeneous environments may not be predictable from genetic variation measured in any single environment.

genetics↗

bioRxiv2025

Dpp Scaling is Not the Key to Robust Wing Patterning in Drosophila

Individuals within a population can vary dramatically in body and trait size in response to environmental factors such as developmental nutrition, temperature, and oxygen level, a phenomenon called phenotypic plasticity. Despite this variation, morphological pattern across the body and within traits are largely maintained, an example of developmental robustness. Consequently, the same trait can display both plastic and robust phenotypes. A fundamental yet unanswered question in developmental biology is: how do organs achieve plasticity in size while maintaining the robustness of pattern? This question is often answered using the French flag model of cell fate specification1-4. The model argues that cells receive positional information from a gradient of signaling molecules (morphogens) that diffuse from a single location in undifferentiated tissue. Specifically, the model argues that if the gradient is dynamically scale invariant, such that the gradient adjusts proportionally to the size of the tissue as it grows, then pattern is maintained regardless of the tissue size. However, while dynamic scale invariance has been demonstrated in several systems5,6, and explicitly2 or implicitly7,8 used to explain the robustness of pattern when tissue size varies due to environmental factors, this hypothesis has not yet been tested. We used the developing Drosophila wing as a model to test this hypothesis, under environmental conditions that reduce (low developmental oxygen level) and increase (low developmental temperature) adult wing size. We found that scale invariance of morphogen gradients is not observed under non-standard environmental conditions and is therefore not an explanation for robust patterning in the Drosophila wing with environmental variation in wing size.

developmental biology↗

bioRxiv2021

A steroid hormone regulates growth in response to oxygen availability

In almost all animals, physiologically low oxygen (hypoxia) during development slows growth and reduces adult body size1-3. The developmental mechanisms that determine growth under hypoxic conditions are, however, poorly understood. One hypothesis is that the effect of hypoxia on growth and final body size is a non-adaptive consequence of the cell-autonomous effects of hypoxia on cellular metabolism. Alternatively, the effect may be an adaptive coordinated response mediated through systemic physiological mechanisms. Here we show that the growth and body size response to moderate hypoxia (10% O2) in Drosophila melanogaster is systemically regulated via the steroid hormone ecdysone, acting partially through the insulin-binding protein Imp-L2. Ecdysone is necessary to reduce growth in response to hypoxia: hypoxic growth suppression is ameliorated when ecdysone synthesis is inhibited. This hypoxia-suppression of growth is mediated by the insulin/IGF-signaling (IIS) pathway. Hypoxia reduces systemic IIS activity and the hypoxic growth-response is eliminated in larvae with suppressed IIS. Further, loss of Imp-L2, an ecdysone-response gene that suppresses systemic IIS, significantly reduces the negative effect of hypoxia on final body size. Collectively, these data indicate that growth suppression in hypoxic Drosophila larvae is accomplished by systemic endocrine mechanisms rather than direct suppression of tissue aerobic metabolism.

developmental biology↗

bioRxiv2021

Sex-Specific Plasticity Explains Genetic Variation in Sexual Size Dimorphism in Drosophila

The difference in body size between females and males, or sexual size dimorphism (SSD), is almost ubiquitous, and yet we have a remarkably poor understanding of the developmental-genetic mechanisms that generate it. Such an understanding is important if we are to distinguish between the many theoretical models of SSD evolution. One such model is the condition dependence hypothesis, which proposes that the body size of the larger sex is also more environmentally sensitive, a phenomenon called sex-specific plasticity (SSP). Because SSP generates differences in female and male body size, selection on plasticity may underlie the evolution of sexual size dimorphism. To test this hypothesis, however, we need to know the genetic architecture of both SSD and SSP, which is challenging because both are characteristics of populations not individuals. Here, we overcome this challenge by using isogenic lineages of Drosophila to measure both SSD and SSP for a genotype. We demonstrate extensive genetic variation for SSD among genotypes that is tightly correlated with variation in SSP, indicating that the same developmental-genetic mechanisms regulate both phenomena. These data support the condition dependence hypothesis and suggest that the observed SSD is a consequence of selection on the developmental-genetic mechanisms that regulate SSP.

evolutionary biology↗

bioRxiv2020

Sex-specific plasticity and the nutritional geometry of insulin-signaling gene expression in Drosophila melanogaster

1.BackgroundSexual-size dimorphism (SSD) is replete among animals, but while the selective pressures that drive the evolution of SSD have been well studied, the developmental mechanisms upon which these pressures act are poorly understood. Ours and others research has shown that SSD in Drosophila reflects elevated levels of nutritional plasticity in females versus males, such that SSD increases with dietary intake and body size, a phenomenon called sex-specific plasticity (SSP). Additional data indicate that while body size in both sexes responds to variation in protein level, only female body size is sensitive to variation in carbohydrate level. Here we explore whether these difference in sensitivity at the morphological level are reflected by differences in how the insulin/IGF-signaling (IIS) and TOR-signaling pathways respond to changes in carbohydrates and proteins in females versus males, using a nutritional geometry approach. ResultsThe IIS-regulated transcripts of 4E-BP and InR most strongly correlated with body size in females and males respectively, but neither responded to carbohydrate level and so could not explain the sex-specific response to body size to dietary carbohydrate. Transcripts regulated by TOR-signaling did, however, respond to dietary carbohydrate in a sex-specific manner. In females, expression of dILP5 positively correlated with body size, while expression of dILP2,3 and 8, was elevated on diets with a low concentration of both carbohydrate and protein. In contrast, we detected lower levels of dILP2 and 5 protein in the brains of females fed on low concentration diets. We could not detect any effect of diet on dILP expression in males. ConclusionAlthough females and males show sex-specific transcriptional responses to changes in protein and carbohydrate, the patterns of expression do not support a simple model of the regulation of body-size SSP by either insulin-or TOR-signaling. The data also indicate a complex relationship between carbohydrate and protein level, dILP expression and dILP peptide levels in the brain. In general, diet quality and sex both affect the transcriptional response to changes in diet quantity, and so should be considered in future studies that explore the effect of nutrition on body size.

developmental biology↗

bioRxiv2017

Which line to follow? The utility of different line-fitting methods to capture the mechanism of morphological scaling

Bivariate morphological scaling relationships describe how the size of two traits co-varies among adults in a population. In as much as body shape is reflected by the relative size of various traits within the body, morphological scaling relationships capture how body shape varies with size, and therefore have been used widely as descriptors of morphological variation within and among species. Despite their extensive use, there is continuing discussion over which line-fitting method should be used to describe linear morphological scaling relationships. Here I argue that the best line-fitting method is the one that most accurately captures the proximate developmental mechanisms that generate scaling relationships. Using mathematical modeling, I show that the best line-fitting method depends on the pattern of variation among individuals in the developmental mechanisms that regulate trait size, and the morphological variation this pattern of developmental variation produces. For Drosophila traits, this pattern of variation indicates that major axis regression is the best line-fitting method. For morphological traits in other animals, however, other line-fitting methods may be more accurate. I provide a simple web-based application for researchers to explore how different line-fitting methods perform on their own morphological data.

evolutionary biology↗