Abstract

Alexandrium pacificum is one of the main species responsible for harmful algal blooms, posing serious threats to coastal ecosystems, economies, and public health. Light intensity is an important abiotic factor affecting the occurrence of red tides. In a certain range, increasing light intensity can promote the rapid growth of A. pacificum. This study aimed to elucidate the molecular mechanisms of H3K79 methylation (H3K79me) in response to high light intensity during the rapid growth of A. pacificum and the formation of toxic red tides. The research found that the abundance of H3K79me increased 2.1-fold under high light (HL, 60 μmol photon m−2 s−l) compared to control light conditions (CT, 30 μmol photon m−2 s−l), which was consistent with the trend of rapid growth under HL, and both can be inhibited by EPZ5676. Then effector genes of H3K79me under HL were identified using ChIP-seq and a virtual genome constructed based on transcriptome data of A. pacificum for the first time. The results showed that the differential modification-associated genes were primarily enriched in the pathways of “energy metabolism”, “carbon metabolism”, and “amino acid metabolism”. These findings were confirmed through ChIP-qPCR. Subsequently, H3K79me-associated genes CP43 and GOGAT were identified by combined analysis of ChIP-seq and differentially expressed genes. Finally, pharmacological experiments using the H3K79me inhibitor EPZ5676 showed that the expression of the photosynthesis-related gene CP43 was significantly reduced by 2.5-fold and the maximum photochemical quantum efficiency of A. pacificum was reduced by 1.2 to 1.8-fold in HL compared with CT, leading to inhibited growth of A. pacificum. These results suggest that H3K79me plays a role in regulating the rapid growth of A. pacificum and photosynthesis is likely an important regulatory pathway, which is the first to provide epigenetic evidence underlying the formation of toxic red tides from the perspective of H3K79me.

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