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Thus, we propose that developmental hormones may provide a mechanistic link between climate change and organismal adaptation. In addition, because developmental hormones often respond to environmental changes, we discuss how endocrine regulation of postembryonic development may impact how organisms evolve in response to climate change. We present a model called a developmental goblet, which provides a visual representation of how metamorphic organisms might evolve. Because of these actions of hormones, metamorphic hormones can shape the evolution of metamorphic organisms. Across generations, the many effects of hormones can bias and at times constrain the evolution of traits during metamorphosis yet, hormonal systems can overcome constraints through shifts in timing of, and acquisition of tissue specific responses to, endocrine regulation. Within an individual’s life cycle, metamorphic hormones respond readily to environmental conditions and alter adult phenotypes. We argue that developmental hormones facilitate the evolution of novel phenotypic innovations and timing of life history events by genetic accommodation. These results suggest that the resultant mosaic phenotype of female neotenics is due to modular responses of different body parts to hormonal actions. Moreover, expression analyses, supported by reverse genetic experiments, showed that EcR and E93 were specifically upregulated in genital sternites (EcR and E93) and ovaries (E93) and required for the development of imaginal characters.
In contrast, ecdysone-related genes (EcR and E93) were upregulated at both neotenic and alate differentiation, suggesting that the heterochronic actions of ecdysone and JH lead the neotenic differentiation. JH titer and expression of one of the downstream genes (Kr-h1) were shown to be temporarily lowered, but increased just prior to the molt into neotenics, while consistently lowered in imaginal molt (i.e., alate differentiation). In this study, by inducing female neotenic differentiation in a damp-wood termite Hodotermopsis sjostedti, morphological investigations together with juvenile hormone (JH) quantification and expression/functional analyses of genes responsible for molting and/or metamorphosis were carried out. Therefore, the question of whether neotenics are larvae or imagos is still under debate. Furthermore, supplementary reproductives that appear when the original queens and kings die or become senescent, exhibit larval features such as winglessness, and are called neotenics. In termites, only reproductives derived from alates are imagos and other sterile castes (including developmentally-terminal soldier caste) are basically juveniles or nymphs. However, it is not fully understood how the mechanisms of molting/metamorphosis are regulated in the course of differentiation between reproductive and sterile castes.
In termites, i.e., hemimetabolous eusocial insects, caste fate is determined during postembryonic development. In termites, it was predicted that the MEKRE93 pathways contribute to caste differentiation (Korb and Belles, 2017 Miura and Maekawa, 2020 Oguchi et al., 2021), and although JH related genes (Met and Kr-h1) were investigated in detail (e.g., Zhou et al., 2007 Saiki et al., 2014 Masuoka et al., 2015Masuoka et al.,, 2018Milacek et al., 2021), the roles of these pathways especially in the neotenic differentiation were not fully understood.Ĭaste development in social insects requires the coordination of molting and metamorphosis during postembryonic development. Specifically, the antimetamorphic action of Kr-h1 is reciprocally repressed by the expression of E93, which is regulated by ecdysone and its receptor (EcR) and the master trigger of imaginal molt and neoteny (Ureña et al., 2014 Bell es and Santos, 2014 Kayukawa et al., 2017 Chafino et al., 2018 Vea et al., 2019). Briefly, after JH binds to the receptor Methoprene-tolerant (Met), this complex upregulates the expression of Krüppel-homolog 1 (Kr-h1), which is known as the transducer of the antimetamorphic signal of JH (Minakuchi et al., 2008(Minakuchi et al.,, 2009Charles et al., 2011 Jindra et al., 2021 Kayukawa et al., 2012).