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Plant organs exhibit a unimodal growth response to temperature, yet the mechanistic links connecting growth-promoting and growth-inhibiting thermal ranges remain unresolved. In Arabidopsis seedlings, warm temperatures promote hypocotyl elongation by relieving phytochrome B (phyB) inhibition, thereby activating the transcription factors PIF4 and PIF7 to drive auxin synthesis. Here, we demonstrate that temperatures beyond the growth optimum actively suppress growth by downregulating auxin levels, auxin signalling, and PIF4 abundance specifically within the cotyledons, the primary site of auxin production. Strikingly, whereas warm temperatures induce the shrinking of phyB nuclear bodies, heat stress causes phyB to assemble into enlarged condensates, a behaviour faithfully recapitulated in mammalian cells, demonstrating an intrinsic biophysical mechanism. Together, our findings indicate that heat-induced growth inhibition is not merely passive stress damage, but an active molecular reversal of the promotive pathway of thermomorphogenesis.
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Bianchimano et al. (2026) studied this question.
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