Krüppel homolog 1 and E93: The doorkeeper and the key to insect metamorphosis

This is the authors' abstract. We don't add key points for this paper.

Insect metamorphosis is regulated by two main hormones: ecdysone (20E), which promotes molting, and juvenile hormone (JH), which inhibits adult morphogenesis. The transduction mechanisms for the respective hormonal signals include the transcription factors Krüppel homolog 1 (Kr-h1) and E93, which are JH- and 20E-dependent, respectively. Kr-h1 is the main effector of the antimetamorphic action of JH, while E93 is a key promoter of metamorphosis. The ancestral regulatory axis of metamorphosis, which operates in insects with hemimetabolan (gradual) metamorphosis and is known as the MEKRE93 pathway, is based on Kr-h1 repression of E93. In the last juvenile stage, when the production of JH dramatically decreases, Kr-h1 expression is almost completely interrupted, E93 becomes upregulated and metamorphosis proceeds. The holometabolan (complete) metamorphosis mode of development includes the peculiar pupal stage, a sort of intermediate between the final larval instar and the adult stage. In holometabolan species, Broad-Complex (BR-C) transcription factors determine the pupal stage and E93 stimulates the expression of BR-C in the prepupa. The MEKRE93 pathway is conserved in holometabolan insects, which have added the E93/BR-C interaction loop to the ancestral (hemimetabolan) pathway during the evolution from hemimetaboly to holometaboly.