MicroRNAs (miRNAs) are involved in the regulation of a number of processes associated with metamorphosis, either in the less modified hemimetabolan mode or in the more modified holometabolan mode. The miR-100/let-7/miR-125 cluster has been studied extensively, especially in relation to wing morphogenesis in both hemimetabolan and holometabolan species. Other miRNAs also participate in wing morphogenesis, as well as in programmed cell and tissue death, neuromaturation, neuromuscular junction

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... ation, and neuron cell fate determination, typically during the pupal stage of holometabolan species. A special case is the control of miR-2 over Kr-h1 transcripts, which determines adult morphogenesis in the hemimetabolan metamorphosis. This is an elegant example of how a single miRNA can control an entire process by acting on a crucial mediator; however, this is a quite exceptional mechanism that was apparently lost during the transition from hemimetaboly to holometaboly. Endocrine regulation of metamorphosis is based on two hormones: (a) 20-hydroxyecdysone (20E), which is the most common biologically active form of ecdysone, and (b) juvenile hormone ( JH). Mostly, 20E promotes molting, whereas JH prevents metamorphosis; thus, when 20E acts in concert with JH, molting leads to a juvenile stage, and when it acts in the virtual absence of JH it triggers metamorphosis (52). At the molecular scale, both hormones act through a cascade of transcription factors that transduce the hormonal signal. In the case of 20E, its heterodimeric receptor is composed of two nuclear receptors: the ecdysone receptor (EcR), to which 20E actually binds, and the ultraspiracle (USP). Upon binding, the 20E-receptor complex activates the expression of a hierarchy of genes that code for transcription factors (e.g., HR3, HR4, HR39, Broad complex, E75, and FTZ-F1). These transcription factors in turn lead to the regulation of genes that determine the cellular changes associated with molting and metamorphosis (26, 35).