ArticlePest management science2026
A glucose-AMPK-FoxO-vestigial signaling axis underlies host sugar-mediated wing dimorphism in Laodelphax striatellus.
Article in Pest management science, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundPhenotypic plasticity in insect wing dimorphism mediates a key trade-off between dispersal and reproduction, but how host plant nutritional cues are transduced into discrete developmental outcomes remains unclear. We investigated the role of glucose in the regulation of wing morph fate in the small brown planthopper (SBPH, Laodelphax striatellus), and the underlying mechanisms were also explored.
resultsElevating glucose via root supplementation or direct injection promotes long-winged (LW) morphs, whereas blocking sugar hydrolysis (via Validamycin A) or glucose availability (via RNAi) induces short-winged (SW) morphs, confirming glucose as the proximate nutritional cue. Mechanistically, glucose signals through the conserved energy sensor AMP-activated protein kinase (AMPK). Low glucose activates AMPK, which directly interacts with the transcription factor Forkhead box O (FoxO) to drive its nuclear translocation. Nuclear FoxO represses expression of the wing master regulator vestigial (Vg), triggering SW development. Conversely, high glucose suppresses AMPK activity, sequesters FoxO in the cytoplasm, and derepresses Vg to induce LW morphs.
conclusionThe glucose-AMPK-FoxO-Vg signaling axis regulates wing dimorphism in SBPH in response to host-derived sugar. The data reveals a previously unrecognized role of AMPK in insect phenotypic plasticity and provides a mechanistic framework linking environmental nutrition to adaptive life-history strategies. © 2026 Society of Chemical Industry.
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