In flowering plants, hydration of desiccated pollen grains on stigma is a prerequisite for pollen germination, during which pollen increase markedly in volume through water uptake, requiring them to survive hypoosmotic shock to maintain cellular integrity. However, the mechanisms behind the adaptation of pollen to this hypoosmotic challenge are largely unknown. Here, we identify the Qc-SNARE protein SYP72, which is specifically expressed in male gametophytes, as a critical regulator of pollen survival upon hypoosmotic shock during hydration. SYP72 interacts with the MSCS-LIKE 8 (MSL8) and is required for its localization to the plasma membrane. Intraspecies and interspecies genetic complementation experiments reveal that SYP72 paralogs and orthologs from green algae to angiosperms display conserved molecular functions and rescue the defects of Arabidopsis syp72 mutant pollen facing hypoosmotic shock following hydration. Our findings demonstrate a critical role for SYP72 in pollen resistance to hypoosmotic shock through the MSL8 cascade during pollen hydration.

Although asymmetric subgenomic epigenetic modification and gene expression have been revealed in the successful establishment of allopolyploids, the changes in chromatin accessibility and their relationship with epigenetic modifications and gene expression are poorly understood. Here, we synthetically analyzed chromatin accessibility, four epigenetic modifications and gene expression in natural allopolyploid Brassica napus, resynthesized allopolyploid B. napus, and diploid progenitors (B. rapa and B. oleracea). “Chromatin accessibility shock” occurred in both allopolyploidization and natural evolutionary processes, and genic accessible chromatin regions (ACRs) increased after allopolyploidization. ACRs associated with H3K27me3 modifications were more accessible than those with H3K27ac or H3K4me3. Although overall chromatin accessibility may be defined by H3K27me3, the enrichment of H3K4me3 and H3K27ac and depletion of DNA methylation around transcriptional start sites up-regulated gene expression. Moreover, we found that subgenome Cn exhibited higher chromatin accessibility than An, which depended on the higher chromatin accessibility of Cn-unique genes but not homologous genes.