While the ultimate causes and adaptive significance of sexual size dimorphism (SSD) have been extensively studied, the developmental mechanisms behind this phenomenon have received little attention. Going through an additional larval instar may form a specific way of achieving SSD in arthropods. In the present study, the mechanisms of SSD determination of two lymantriid moths, with marked SSD, were studied. In both species, females tended to go through an additional instar compared to males, and form pupae that were more than twice the weight of the males. To reveal the role of an extra instar, larval growth was monitored in the laboratory and the growth parameters were analysed as dependent on sex and developmental type (number of instars). Prolongation of growth by means of adding an additional larval instar in females turned out to be the key mechanism in the determination of the highly female-biased SSD in the species studied. There is thus a developmental mechanism available that permits achieving a larger size by means of extending the growth period. This provides evidence against constraint-based evolutionary explanations for body sizes in insects. There was no considerable accumulation of SSD during earlier larval life when females went through more instars than males. In contrast, in those cases in which males and females had the same number of instars, SSD accumulated gradually during the course of several larval instars. Longer growing period turned out to be a crucial mechanism leading to the female-biased SSD even when instar number did not differ between sexes, although higher instantaneous relative growth rates of females also played a complementary role in the latter case. Within sexes, an additional instar was characteristic of initially smaller larvae, as predicted by the "threshold size" hypothesis.
A series of experiments were conducted to compare the susceptibility of P. regina larvae reared in isolation or in groups to the effects of diet-borne metabolic inhibitors: chlorogenic acid (CGA) and mimosine. Larvae were presented with diets containing 0.4 mM CGA or 0.4 mM CGA in combination with 22 mM lysine or methionine or with diets containing 1.5, 15 or 30 mM concentrations of mimosine. Methionine and CGA caused significantly reduced pupal weights when compared with larvae presented with lysine and CGA. All concentrations of mimosine resulted in 100% mortality with larvae unable to successfully complete pupation even at the lowest concentration. In general, larvae reared in groups were less susceptible to the toxic effects resulting from diet-borne metabolic inhibitors. The results are discussed in relation to the chemical factors that result from the feeding activity of saprophagous dipterans.