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Low phosphate represses histone deacetylase complex1 to regulate root system architecture remodeling in Arabidopsis.

Whilst the mechanisms involved in the regulation of gene expression in response to phosphate (Pi) deficiency have been extensively studied, their chromatin-level regulation remains poorly understood. We examined the role of histone acetylation in response to Pi deficiency by using histone deacetylase complex1 (hdc1) mutant. Genes involved in root system architecture (RSA) remodeling were analyzed by quantitative real-time PCR (qPCR) and chromatin immunoprecipitation qPCR. We demonstrate that histone H3 acetylation increased under Pi deficiency, and the hdc1 mutant was hypersensitive to Pi deficiency, with primary root growth inhibition and root hair number increases. Concomitantly, Pi deficiency repressed HDC1 protein levels. Under Pi deficiency, hdc1 accumulated higher levels of Fe3+ in the root tips and had higher expression of genes involved in RSA remodeling such as ALUMINUM-ACTIVATED MALATE TRANSPORTER1 (ALMT1), and LOW PHOSPHATE ROOT1 (LPR1), and LPR2 than wild-type plants. Furthermore, Pi deficiency enriched the histone H3 acetylation of ALMT1 and LPR1. Finally, genetic evidence showed that LPR1/2 was epistatic to HDC1 in regulating RSA remodeling. Our results suggest a chromatin-level control of Pi starvation responses in which HDC1-mediated histone H3 deacetylation represses the transcriptional activation of genes involved in RSA remodeling in Arabidopsis.