Disruption of OsPHD1, Encoding a UDP-Glucose Epimerase, Causes JA Accumulation and Enhanced Bacterial Blight Resistance in Rice

Abstract

Lesion mimic mutants (LMMs) have been widely used in experiments in recent years for studying plant physiological mechanisms underlying programmed cell death (PCD) and defense responses. Here, we identified a lesion mimic mutant, <i>lm212-1</i>, which cloned the causal gene by a map-based cloning strategy, and verified this by complementation. The causal gene, <i>OsPHD1</i>, encodes a UDP-glucose epimerase (UGE), and the <i>OsPHD1</i> was located in the chloroplast. <i>OsPHD1</i> was constitutively expressed in all organs, with higher expression in leaves and other green tissues. <i>lm212-1</i> exhibited decreased chlorophyll content, and the chloroplast structure was destroyed. Histochemistry results indicated that H₂O₂ is highly accumulated and cell death is occurred around the lesions in <i>lm212-1</i>. Compared to the wild type, expression levels of defense-related genes were up-regulated, and resistance to bacterial pathogens <i>Xanthomonas oryzae pv. oryzae</i> (<i>Xoo</i>) was enhanced, indicating that the defense response was activated in <i>lm212-1</i>, ROS production was induced by flg22, and chitin treatment also showed the same result. Jasmonic acid (JA) and methyl jasmonate (MeJA) increased, and the JA signaling pathways appeared to be disordered in <i>lm212-1</i>. Additionally, the overexpression lines showed the same phenotype as the wild type. Overall, our findings demonstrate that <i>OsPHD1</i> is involved in the regulation of PCD and defense response in rice.