When summers are hotter and heat waves occur more often and last longer, the consequences can be severe. While warmth can boost the growth of plants, heat stress can restrict their growth and flowering.
Brigitte Poppenberger, PhD, professor of biotechnology of horticultural crops at the Technical University of Munich (TUM) in Freising, Germany said, “Heat stress can negatively affect plants in their natural habitats and destabilize ecosystems while also drastically reducing crop harvests, thereby threatening our food security.”
Acute, sub-lethal heat stress triggers an ancient molecular defense pathway in all organisms called the “heat shock response” that protects plants and animals from proteotoxic stress that damages proteins. One of the ways in which the heat shock response works is by producing proteins called “heat shock proteins” that act as molecular guides that ensure proteins fold properly into their complex, three-dimensional functional conformations.
Earlier studies showed a steroid hormone called brassinosteroid, which promotes plant growth, plays a role in heat stress signaling but the underlying mechanism was not known.
In a new study published in The EMBO Journal titled, “Transcription factor BES1 interacts with HSFA1 to promote heat stress resistance of plants,” researchers at TUM claim to have discovered what contributes to the protective ability of brassinosteroids.
The activity of brassinosteroids is controlled by a sub-family of DNA binding transcription factors called BES1/BZR1 that can flip the switch for decoding the genetic code from off to on and vice versa. In this study, Poppenberger’s team used a small flowering plant model that grows in temperate climates (Arabidopsis thaliana, thale cress) to provide evidence that BES1 contributes to heat stress signaling, clarifying how brassinosteroids protect against heat stress.
The researchers showed BES1 interacts with another class of DNA binding transcription factors called heat shock factors to increase synthesis of heat shock proteins. Therefore, when BES1 activity increases, plants become more resistant to heat stress, and when its activity decreases they become more sensitive to rising temperatures.
“We present an alternative mode of BES1 activity, which allows BES1 to be recruited to the heat shock response pathway,” the authors noted.
Using biochemical assays, the authors showed heat stress dephosphorylates BES1 to activate it. They found that this activation does not require the presence of brassinosteroids and identified the enzymes that mediate BES1’s dephosphorylation. The researchers also showed that BES1 directly binds to heat shock elements—binding sites on DNA for heat shock factors. The study found that the activation of BES1 by heat stress is stimulated by brassinosteroids.
“These findings lead us to propose an extended model of the heat stress response in plants, in which the recruitment of BES1 is a means of heat stress signaling cross-talk with a central growth regulatory pathway,” the authors wrote.
Poppenberger added, “These results are not only of interest to biologists trying to expand our understanding of the heat shock response but also have potential for practical application in agriculture and horticulture.”
For instance, brassinosteroids can be used in bio-stimulant sprays to increase resistance to heat stress in plants. Being a natural substance, such products would be approved for organic farming and remain to be tested for their efficacy in different crop plants. In a parallel approach, targeting BES1 through plant breeding could help develop crop varieties that are more resistant to future heat waves.