Biology subjects

Frankino, W. A.

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

5 recordsLinked to original sources

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↗

bioRxiv2026

Embryonic environment impacts adult traits and phenotypic integration in the pea aphid

Understanding how the embryonic environment affects adult phenotype is critical in the context of both human health and the increasing variance of environmental conditions due to climate change. Here we consider this topic within the framework of phenotypic integration, i.e., the pattern of correlations among elements of functionally robust trait suites. We investigated the life-long consequences of alternative embryonic environments on phenotypic integration in the pea aphid (Acyrthosiphon pisum). We exposed live-bearing pea aphid mothers to an adverse, high-density environment or a benign, low-density environment and measured morphological traits, fecundity, and transcriptional profiles in the resulting winged and wingless adult offspring. We observe that morphological integration decreases in both morphs in response to the adverse maternal environment. Transcriptional integration, on the other hand, shows a morph-specific response: integration increases in wingless offspring but decreases in winged offspring in response to the adverse maternal environment. Our results show the remarkable phenotypic diversity that a single genotype can express in response to environmental variation; that maternal environmental conditions can have strong effects on offspring trait variation and trait integration; and that these effects differ at the morphological and transcriptional levels.

evolutionary biology↗

bioRxiv2025

Private QTLs and the Genetic Architecture of Hierarchical Size Traits: From Body Size to Sex-Specific Plasticity

Sex-specific size plasticity (SSP) is the phenomenon whereby the size of one sex is more environmentally sensitive than the other, and is thought to underlie the developmental regulation and evolution of sexual size dimorphism (SSD). Sex-specific plasticity is a higher order phenotype that emerges due to the effect of the environment and sex on core growth regulatory mechanisms. Genetic variation in SSP necessarily requires sex- and environment-specific variation in growth, yet the developmental-genetic mechanisms enabling such context-dependent size variation remain poorly understood. Using a genome-wide association study (GWAS) and functional validation in Drosophila melanogaster, we dissected the genetic architecture of body size, size plasticity, SSD, and SSP across 196 isogenic lineages. We find that each phenotype is governed by largely non-overlapping sets of loci, with most candidate variants lying outside canonical growth pathways. Instead, size trait are shaped by "private QTLs", whose effects are limited to specific sex, trait, or environmental contexts. Functional knockdown of selected candidate genes for SSP revealed that while most did not affect SSP directly, many influenced body size, SSD, and size plasticity, in a manner consistent with their nested phenotypic relationships. Together, our results suggest that context-dependent alleles in genes peripheral to core growth regulatory pathways drive variation in SSD and SSP, offering a mechanistic explanation for their evolutionary lability and highlighting the role of private QTLs in structuring complex trait architecture. Significance StatementSexual size dimorphism (SSD), the differences in body size between females and males, is highly variable among species and yet the developmental genetic mechanisms that generate it and drive its evolution remain elusive. Our work reveals a modular genetic architecture underlying SSD in Drosophila melanogaster, showing that variation in body size, its sex-specific plasticity, and the resulting SSD are controlled by largely non-overlapping, context-dependent loci. This finding provides critical insight into how complex morphological differences between the sexes are genetically organized, allowing for the flexible and independent evolution of hierarchical traits.

evolutionary biology↗

bioRxiv2022

The Genetic Architecture of Morphological Scaling

Morphological scaling relationships between the sizes of individual traits and the body captures the characteristic shape of a species, and the evolution of scaling is the primary mechanism of morphological diversification. However, we have almost no knowledge of the genetic architecture of scaling, critical if we are to understand how scaling evolves. Here we explore the genetic architecture of population-level morphological scaling relationships - the scaling relationship fit to multiple genetically-distinct individuals in a population - by describing the distribution of individual scaling relationships - genotype-specific scaling relationships that are unseen or cryptic. These individual scaling relationships harbor the genetic variation that determines relative trait growth within individuals, and theoretical studies suggest that their distribution dictates how the population scaling relationship will respond to selection. Using variation in nutrition to generate size variation within 197 isogenic lineages of Drosophila melanogaster, we reveal extensive variation in the slopes of the wing-body and leg-body scaling relationships among individual genotypes. This genetic variation reflects variation in the nutritionally-induced size plasticity of the wing, leg and body. Surprisingly, we find that variation in the slope of individual scaling relationships primarily results from variation in nutritionally-induced plasticity of body size, not leg or wing size. These data allow us to predict how different selection regimes alter scaling in Drosophila and is the first step in identifying the genetic targets of such selection. More generally, our approach provides a framework for understanding the genetic architecture of scaling, an important prerequisite to explaining how selection changes scaling and morphology.

genetics↗

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↗