Insect silk glands: their types, development and function, and effects of environmental factors and morphogenetic hormones on them

Abstract

Insect silk glands are ectodermal organs that evolved several times in the phylogeny from one of the following cell types: epidermal cells associated with bristle formation; sex accessory glands; larval Malpighian tubules; and larval labial salivary glands. As far as is known, the ultrastructure of the silk-producing cells is similar in all gland types, except for the labial glands of lower Hymenoptera. In most Lepidoptera and Trichoptera, the posterior gland region secretes fibroin and one to several small proteins; this core of silk is enveloped in the middle region of the gland by a mixture of sericins. The cuticle-lined anterior region provides the gland outlet. Lepidopteran silk glands become secretory prior to hatching. During larval life they increase their secretory potential by growing in size and ploidy. Their function fluctuates in each instar according to a “larval” pattern, which is characterized by the initiation of intensive RNA transcription with the resumption of feeding, by a high rate of proteosynthesis during feeding, and by cessation of these activities with the advancement of the next molt. In the last-larval instar, the silk glands develop according to a metamorphic pattern that differs from the larval one by enhanced function and, especially, by the programming of silk glands for histolysis. Starvation of larvae causes silk gland regression, cold shock prevents spinning, and exposure of larvae to alcohol vapours kills certain silk gland cells. Development of silk glands is altered with hormonal treatments of larvae. Juvenile hormone (JH) curbs silk gland function, prevents their degeneration, and, indirectly, it can cause an increase in silk production. Low doses of ecdysteroids accelerate silk gland development to increased function, while high doses cause regression and degeneration. Juvenile hormone anologues and anti-JH compounds are used in sericulture to control the yield and quality of silk. Available data are consistent with the following scheme of the hormonal control of silk glands. The change from the larval to the metamorphic developmental pattern is caused by a drop in JH titre. Realization of the pattern depends on consecutive action of several factors: trace amounts of JH in the last-larval instar affect silk glands via regulation of feeding and molt timing; function of silk glands depends on nutrient supply and it is stimulated by a brain neurohormone; slight elevation of ecdysteroid titre, which is associated with the termination of feeding and initiation of cocoon spinning, may be implicated in the culmination of proteosynthesis, and in the initiation of functional regression in the silk glands; the molt-inducing surge of ecdysteroids induces regression in the silk glands developing according to the larval pattern, but degeneration in those completing the metamorphic developmental pattern.