A research team led by Prof. XIAO Jun at the Institute of Genetics and Developmental Biology (IGDB), Chinese Academy of Sciences, has uncovered a novel mechanism by which temperature shapes plant cell fate via epigenetic regulation. Their study, published online in Developmental Cell on April 22, reveals how environmental temperature modulates key chemical marks on chromatin—the complex of DNA and proteins that governs gene activity—thereby influencing cell identity.

Focusing on the model plant Arabidopsis thaliana, the researchers examined the critical transition from seed to seedling. This phase requires the permanent silencing of embryonic genes to ensure proper growth. Two major protein complexes, Polycomb Repressive Complexes 1 and 2 (PRC1 and PRC2), play a central role in this silencing. PRC2 places a repressive epigenetic mark known as H3K27me3 on histone proteins, while PRC1 adds similar tags—H2Aub or H2A.Zub—to the histone H2A or its variant H2A.Z. These modifications compact the chromatin structure, rendering embryonic genes inaccessible and keeping them switched off after germination.

However, when PRC1 or PRC2 function is disrupted, repression of key developmental genes (such as LEC1 and ABI3) is lost, leading to de-differentiation and the re-acquisition of embryonic traits—essentially returning cells to a pluripotent, callus-like state. This phenomenon illustrates Waddington’s concept of developmental plasticity, where epigenetic landscapes can be reshaped in response to internal or external signals.

Strikingly, the team discovered that low ambient temperatures (16 °C) can partially compensate for PRC2 deficiency, restoring developmental balance in PRC2 mutants. Through integrated transcriptomic, epigenomic, and genetic analyses, they identified TOE1, a transcription factor, as a key temperature-responsive regulator. 

This compensatory mechanism reveals a sophisticated layer of temperature-sensitive epigenetic reprogramming that ensures developmental continuity under environmental stress. The findings offer a promising strategy for optimizing callus induction and crop regeneration through simple manipulation of culture temperatures.

Beyond plant biology, the study emphasizes the evolutionary conservation of the H3K27me3 mark across eukaryotes. In plants, it balances developmental flexibility and environmental responsiveness. In animals, it safeguards cell identity and prevents inappropriate de-differentiation. In humans, misregulation of H3K27me3—such as in cancer—can reactivate stem-like programs, echoing the callus formation observed in plants.

Ultimately, this work reinforces the view that the genome is not a static blueprint but a dynamic interface between environmental cues and epigenetic regulation. Insights from temperature-induced reprogramming in plants may even inform future therapeutic approaches to cancer and regenerative medicine.

Source: https://english.cas.cn/newsroom/research_news/life/202504/t20250427_1042096.shtml