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Sclerotinia sclerotiorum hijacks copper from its host for infection

D. Yijuan, J. Mei, Y. Chai, W. Yang, Y. Mao, B. Yan, Y. Yu, J. O. Disi, K. Rana, J. Li, W. Qian

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Abstract

Sclerotinia sclerotiorum induces host reactive oxygen species (ROS) production, which leads to necrosis in the host, allowing the pathogen to absorb nutrients from the dead tissues. Here, we found that three S. sclerotiorum genes involved in copper ion import/transport, SsCTR1, SsCCS and SsATX1, were significantly up-regulated during infection of Brassica oleracea. Function analysis revealed that these genes involved in fungal ROS detoxification, oxalic acid production, pathogen establishment and virulence. On the host side, four genes putatively involved in copper ion homeostasis, BolCCS, BolCCH, BolMT2A and BolDRT112, were significantly down-regulated in susceptible B. oleracea, but stably expressed in resistant B. oleracea during infection. Their homologs were found to promote resistance to necrotrophic pathogens and increase antioxidant activity in Arabidopsis thaliana. Furthermore, copper concentration analysis indicated that copper is transported into the necrotic area from healthy area during infection. Collectively, our data suggest that S. sclerotiorum hijacks host copper to detoxify ROS, whereas the resistant hosts restrict the supply of essential copper nutrients to S. sclerotiorum by maintaining copper ion homeostasis during infection.

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