Abstract

Abstract The developmental origin of phenotypic plasticity in morphological shape can be attributed to environment-specific changes in growth of overall body size, localized growth of a morphological structure or a combination of both. I monitored morphological development in the first four nymphal instars of grasshoppers (Melanoplus femurrubrum) raised on two different plant diets to determine the ontogenetic origins of diet-induced phenotypic plasticity and to quantify genetic variation for phenotypic plasticity. I measured diet-induced phenotypic plasticity in body size (tibia length), head size (articular width and mandible depth) and head shape (residual articular width and residual mandible depth) for grasshoppers from 37 full-sib families raised on either a hard plant diet (Lolium perenne) or a soft plant diet (Trifolium repens). By the second to third nymphal instar, grasshoppers raised on a hard plant diet had significantly smaller mean tibia length and greater mean residual articular width (distance between mandibles adjusted for body size) compared with full-sibs raised on a soft plant diet. However, there was no significant phenotypic plasticity in mean unadjusted articular width and mandible depth, and in mean residual mandible depth. At the population level, development of diet-induced phenotypic plasticity in grasshopper head shape is mediated by plastic changes in allocation to tissue growth that maintain growth of head size on hard, low-nutrient diets while reducing growth of body size. Within the population, there was substantial variation in the plasticity of growth trajectories since different full-sib families developed phenotypic plasticity of residual articular width through different combinations of head and body size growth. Genetic variation for diet-induced phenotypic plasticity of residual articular width, residual mandible depth and tibia length, as estimated by genotype–environment interaction, exhibited significant fluctuation through ontogeny (repeated measures MANOVA, family × plant × instar, P < 0.01). For example, there was significant genetic variation for phenotypic plasticity of residual articular width in the third nymphal instar, but not earlier or later in ontogeny. The observed patterns of genetic variation are discussed with reference to short-term constraints and the evolution of phenotypic plasticity.

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