Document Type


Publication Date



A biochemically based model was developed to simulate the growth, development and metamorphosis of larvae of the Pacific oyster, Crassostrea gigas. The model is unique in that (1) it defines larvae in terms of their protein, neutral lipid, polar lipid, carbohydrate, and ash content; (2) it tracks weight separately from length to follow larval condition index; and (3) it includes genetic variation in growth efficiency and egg quality to better simulate cohort population dynamics. The model includes parameterizations for larval filtration, ingestion, and respiration, which determine growth rate, and processes controlling larval mortality and metamorphosis. The initial biochemical content of the larva is determined by the composition of the egg. Changes in the initial ratios of protein, carbohydrate, neutral lipid, and polar lipid occur in response to the biochemical composition of available food as the larva grows. Modeling the process of metamorphosis requires a series of size-based and biochemically based triggers: (1) larvae become potentially competent to metamorphose at 275 mum, following a decrease in filtration rate at 250 mum; (2) larvae become competent to metamorphose when a daily decline in neutral lipid of 25% or more occurs; and (3) larvae metamorphose successfully if neutral lipid stores exceed polar lipid stores. Although based on simple biochemistry, the model succeeds in simulating such basic characteristics of C. gigas larval development and metamorphosis as larval life span and size structure at metamorphosis and the influence of egg and food quality and food quantity on survival. These results suggest that simple biochemical constructs may encompass the biochemical transitions most prominent in determining cohort success. Simulations of larval development show that for the smallest larvae, assimilation does not provide adequate resources to explain observed growth, although measured filtration rates would indicate otherwise. Egg lipid stores are needed to sustain the larva, The simulations also identify egg sizes in the range 37-73 mum to be viable, very similar to observations. Egg sizes outside this range are predicted to be nonviable due to lipid deficiencies in early larval life. Similarly, simulations identify upper and lower genetic limits on growth efficiency beyond which larvae cannot acquire sufficient neutral lipid stores to successfully metamorphose. As food supply declines, animals with high growth efficiencies are selected in the simulation. Low-protein food diets are predicted to increase larval survival. High-protein diets result in insufficient carbohydrate and neutral lipid to cover metabolic and storage needs. Thus, the influence of growth efficiency is nonrandomly distributed across egg size and respiration rate and the influence seems to be mediated in part by food quantity and to a larger measure by food quality.