H2A.Z removal mediates the activation of genes accounting for cell elongation under light and temperature stress.

The histone variant H2A.Z is crucial for the expression of genes involved in cell elongation under elevated temperatures and shade. Its removal facilitates the activation of these genes, particularly through the activities of PHYTOCHROME INTERACTING FACTORs (PIFs) and the SWR1-related INOSITOL REQUIRING 80 (INO80) complex. Arabidopsis seedlings exhibit rapid elongation of hypocotyls and cotyledon petioles in response to environmental stresses, namely elevated temperatures and shade. These phenotypic alterations are regulated by various phytohormones, notably auxin. Under these stress conditions, auxin biosynthesis is swiftly induced in the cotyledons and transported to the hypocotyls, where it stimulates cell elongation. The histone variant H2A.Z plays a pivotal role in this regulatory mechanism. H2A.Z affects the transcription of numerous genes, particularly those activated by the mentioned environmental stresses. Recent studies highlighted that the eviction of H2A.Z from gene bodies is crucial for the activation of genes, especially auxin biosynthetic and responsive genes, under conditions of elevated temperature and shade. Additionally, experimental evidence suggests that PHYTOCHROME INTERACTING FACTORs (PIFs) can recruit the SWR1-related INOSITOL REQUIRING 80 (INO80) complex to remove H2A.Z from targeted loci, thereby activating gene transcription in response to these environmental stresses. This review provides a comprehensive overview of the regulatory role of H2A.Z, emphasizing how its eviction from gene loci is instrumental in the activation of stress-responsive genes under elevated temperature and shade conditions.