When warmth becomes heat, seedlings reverse a growth-promoting pathway

A growth response changes direction

Why does a seedling grow faster as conditions warm, then slow when temperatures rise further? A new study in Arabidopsis thaliana suggests that parts of the molecular machinery promoting growth in warmth can switch towards restraining it under heat.

Luciana Bianchimano and colleagues describe the findings in a bioRxiv preprint posted on November 9, 2026. The work has not been peer reviewed. It combines measurements of seedling growth, hormone-sensitive reporters, genetic experiments and imaging of plant proteins expressed in mammalian cells.

The researchers focused on the hypocotyl: the young stem section below the seed leaves, or cotyledons. Seedlings initially grown at 22°C were moved to temperatures between 10°C and 37°C on their fourth day. Over the following nine hours, ordinary seedlings showed their greatest hypocotyl elongation at 28°C, with less growth at higher temperatures. That optimum applies to this experiment, not to every plant or growing condition.

Less growth hormone, not an excess

The established warm-temperature pathway starts partly in the cotyledons. Proteins called PIF4 and PIF7 help activate genes involved in producing auxin, a hormone that travels to the hypocotyl and promotes elongation. The light- and temperature-sensing protein phytochrome B, abbreviated phyB, normally restrains this pathway; warmth reduces that restraint.

One possible explanation for growth slowing under stronger heat was that the growth-promoting signal became excessive. The experiments instead supported a reduction in auxin activity.

An auxin sensor in hypocotyl cells and a chemical assay of whole seedlings both indicated that hormone levels peaked at 28°C and declined at 33–37°C. Other reporters showed reduced auxin signalling under hotter conditions. The space outside hypocotyl cells also became more alkaline, rather than showing the excessive acidification predicted by the alternative explanation.

Genetic results reinforced this interpretation. Several mutants impaired in auxin production or downstream growth responses already grew less in warmth and did not show the usual additional decline between 28°C and 37°C. Adding the synthetic auxin Picloram partially restored elongation at 33°C, but did not restore growth at 37°C. The latter result points to additional limits beyond hormone supply.

PIF4 itself behaved differently in different organs. Its abundance fell under heat in the cotyledons, the main auxin-producing site in this pathway, while continuing to rise in the hypocotyl. This selectivity argues against treating the response as a uniform shutdown of growth-related proteins throughout the seedling.

A sensor gathers into larger clusters

The most unexpected finding concerned phyB. This protein can gather into concentrated clusters inside cell nuclei, known as nuclear bodies or condensates. In the mild-to-warm temperature range, these structures generally shrink. Under hotter conditions, however, the researchers observed larger phyB bodies in both hypocotyl and cotyledon cells.

Light treatments helped probe this reversal. Far-red light normally shifts phyB towards its inactive form and encourages the bodies to disperse. Yet large bodies were present after far-red treatment followed by incubation in darkness at 37°C. In one protocol, seedlings kept at 37°C for four hours after a far-red pulse were transferred to 28°C for one hour; their nuclear bodies significantly shrank, showing that maintaining the enlarged structures required sustained heat.

A separate protocol tested whether heat could trigger formation after the bodies had largely dispersed. Following a far-red pulse, seedlings were first kept at 28°C for one hour to allow near-complete disassembly, then transferred to 37°C for four hours. Large bodies formed under these conditions. Together, the two protocols demonstrate shrinkage after cooling and heat-induced assembly after prior disassembly, rather than a heating–cooling–reheating cycle in the same seedlings.

To investigate whether the effect required the surrounding plant machinery, the team expressed phyB in Chinese hamster ovary cells. With a plant interaction partner present, phyB clusters again shrank between 22°C and 28°C and enlarged at 37°C, without a significant change in total nuclear phyB fluorescence in that experiment. A constitutively active phyB variant also formed larger clusters with increasing temperature, including without the partner. These results support an intrinsic contribution from phyB to the assembly response, although mammalian cells are not a protein-only test system.

Evidence for a brake, with limits

Larger clusters and slower growth could merely occur together. To investigate a functional connection, the researchers examined mutations in PCH1 and PCHL, proteins that help phyB form nuclear bodies. Under strong continuous red light at 37°C, impaired body formation was accompanied by greater hypocotyl elongation than in ordinary seedlings.

That supports a role for the assemblies in growth restraint. It does not cleanly isolate their effects, because PCH1 and PCHL have other molecular functions, a challenge the paper acknowledges.

Overall, the findings support an actively regulated contribution to rapid heat-induced growth inhibition. They do not establish that cellular damage never contributes, demonstrate improved survival, or show that the same mechanism governs crop performance during prolonged heat. The central insight is narrower: in these young seedlings, warmth and stronger heat can push a familiar growth-regulating pathway in opposite directions.