ENAP1 retrains seed germination via H3K9 acetylation mediated positive feedback regulation of ABI5

Histone acetylation is involved in the regulation of seed germination. The transcription factor ABI5 plays an essential role in ABA- inhibited seed germination. However, the molecular mechanism of how ABI5 and histone acetylation coordinate to regulate gene expression during seed germination is still ambiguous. Here, we show that ENAP1 interacts with ABI5 and they co-bind to ABA responsive genes including ABI5 itself. The hypersensitivity to ABA of ENAP1ox seeds germination is recovered by the abi5 null mutation. ABA enhances H3K9Ac enrichment in the promoter regions as well as the transcription of target genes co-bound by ENAP1 and ABI5, which requires both ENAP1 and ABI5. ABI5 gene is directly regulated by ENAP1 and ABI5. In the enap1 deficient mutant, H3K9Ac enrichment and the binding activity of ABI5 in its own promoter region, along with ABI5 transcription and protein levels are all reduced; while in the abi5-1 mutant, the H3K9Ac enrichment and ENAP1 binding activity in ABI5 promoter are decreased, suggesting that ENAP1 and ABI5 function together to regulate ABI5- mediated positive feedback regulation. Overall, our research reveals a new molecular mechanism by which ENAP1 regulates H3K9 acetylation and mediates the positive feedback regulation of ABI5 to inhibit seed germination.
Summary To optimize the fitness in natural environment, flowering plants initiate seed germination in the favorable environment and maintain seed dormancy under stressful conditions. Precise mechanisms have been evolved to regulate germination timing to ensure plant adaptation to unfavorable environment. ABA, a major stress hormone in plants, induces seed dormancy and represses seed germination. Epigenetic regulation has been known involved in ABA signaling in which the transcription factor ABI5 acts as a regulatory hub. However, the epigenetic regulation such as histone acetylation on ABI5 transcription remains elusive. In this study, we revealed a new molecular mechanism by which histone binding protein ENAP1 regulates H3K9 acetylation, which mediates the positive feedback regulation of ABI5 in an ABI5 dependent manner to inhibit seed germination.