What it is
Many insects can produce distinct wing forms from a single genotype, depending on their environment. Working in two evolutionarily divergent hemipterans, the firebug Pyrrhocoris apterus and the planthopper Nilaparvata lugens, the authors show that ecdysteroid steroid hormones act as a central switch for wing polyphenism, integrating signals from the prothoracicotropic hormone (PTTH) and its receptor Torso and from insulin/IGF-1 signaling. Silencing ecdysteroid production or receptor components induced wing bud growth, mutating Ptth or Torso turned short-wing-destined wing buds into long wings, and added ecdysteroids neutralized the effect of Torso and insulin/IGF-1 signaling on wing form, redirecting wing development from long to short.
Why it matters
Wing polyphenism is a prevalent evolutionary adaptation in insects, and although the endocrine signals behind it differ between hemipteran lineages, the evolutionarily conserved genetic toolkit underlying this developmental plasticity had remained elusive. Finding the same neuropeptide-ecdysteroid axis in two divergent species points to a conserved regulatory principle for wing polyphenism across Hemiptera.
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Filed underNeurobiology and Insect Physiology Research, Animal Behavior and Reproduction, Developmental Biology and Gene Regulation