Abstract
Phosphate availability is becoming a limiting environmental factor that inhibits plant growth and development. Here, we demonstrated that mutation of the histone acetyltransferase GCN5 impaired phosphate starvation responses (PSRs) in Arabidopsis. Transcriptome analysis revealed that 888 GCN5-regulated candidate genes were potentially involved in responding to phosphate starvation. ChIP assay indicated that four genes, including a long non-coding RNA (lncRNA) At4, are direct targets of GCN5 in PSR regulation. In addition, GCN5-mediated H3K9/14 acetylation of At4 determined dynamic At4 expression. Consistent with the function of At4 in phosphate distribution, mutation of GCN5 impaired phosphate accumulation between shoots and roots under phosphate deficiency condition, whereas constitutive expression of At4 in gcn5 mutants partially restored phosphate relocation. Further evidence proved that GCN5 regulation of At4 influenced the miRNA miR399 and its target PHO2 mRNA level. Taken together, we propose that GCN5-mediated histone acetylation plays a crucial role in PSR regulation via the At4-miR399-PHO2 pathway and provides a new epigenetic mechanism for the regulation of lncRNA in plants.