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Crucial to plant development, ambient temperature triggers intricate mechanisms enabling adaptive responses to temperature variations. The precise coordination of chromatin modifications in shaping cell developmental fate under diverse temperatures remains elusive. Our study, integrating comprehensive transcriptome, epigenome profiling, and genetics, demonstrates that lower ambient temperature (16°C) partially restores developmental defects caused by H3K27me3 loss in prc2 mutants by specifically depositing H2A.Zub at ectopically expressed embryonic genes in Arabidopsis, such as ABA INSENSITIVE 3 (ABI3) and LEAFY COTYLEDON 1 (LEC1). This deposition leads to downregulation of these genes and compensates for H3K27me3 depletion. Polycomb-repressive complex 1 (PRC1)-catalyzed H2A.Zub and PRC2-catalyzed H3K27me3 play roles in silencing transcription of embryonic genes for post-germination development. Low-temperature-induced reduction of TOE1 protein level decelerates H2A.Z turnover at specific loci, sustaining repression of embryonic genes and alleviating requirement for PRC2-H3K27me3 at post-germination stage. Our findings offer mechanistic insights into the cooperative epigenetic layers, facilitating plant adaptation to varying environmental temperatures.