Role of ecdysone in larval metamorphosis

Abstract

Larvae of almost all insects and nematodes have to undergo a cycle of molting for growing and further development, and with the final molt, adults emerge (complete metamorphosis). In insects, it seems that complete metamorphosis takes place through a dormant stage (pupa), in which all larval cells (muscles, salivary glands, gut, etc.) disintegrate by apoptosis. That is why adult forms appear completely different from their pre-pupa larval stages. In contrast, adult nematodes resemble their final larval stages because dormant pupa stages are absent. In insects, molting with or without pupation requires a pro-thoracicotropic hormone (PTTH) secreted by two pairs of cells in the larval brain. This hormone activates prothoracic glands to secrete a steroid hormone, known as the ecdysone. Also by these glands, sufficient production of the juvenile hormone (JH), promotes larva molting. In case of lower JH production, steroid hormones promote pupation, while complete loss of JH leads to direct formation of the adult from the last final larval molt [1]. Steroid hormones have an essential role on the physiological development and behavior of various organisms. Ecdysone is a major steroid hormone that directs major transitions during developmental stages in the life cycle of some helminth and almost all insects by coordinating larval molting and metamorphosis. Ecdysteroid is produced by the prothoracic gland of all insects as 20-hydroxyecdysone. Increase of ecdysteroid induces the expression of genes controlling protein production for larval development. In adult female insects, ecdysone signaling is critical for reproduction as it mediates egg-chamber maturation during oogenesis, whereas in adult males, ecdysteroids have a role in sperm maturation. It is also present in several plants to protect them from agricultural insects. The ecdysone receptor (EcR) is a nuclear receptor found in the cells of reproduction in all insects, and is activated through binding with ecdysteroid. Once activated, it leads to activation of several genes responsible for physiological changes leading to larval ecdysis (molting). EcR is a non-covalent heterodimer of two proteins; EcR protein and ultraspiracle protein (USP), which are homologous to the mammalian farnesoid X receptor (FXR) and retinoid X receptor (RXR) proteins, respectively. The term USP is usually used for the EcR partner from dipteran and lepidopteran insects, while RXR is applied in other insects. This means that EcR consists of EcR protein and USP for dipteran and lepidopteran insects, whereas it consists of EcR protein and RXR for other insects [2-5]. EcR is mainly applied to control gene expression with two uses; for gene therapy in medical and agricultural fields, and for drug development and vector control in Parasitology researches. The present editorial aims to throw light on the second application.