Abstract

Fire blight caused by the gram-negative bacterium Erwinia amylovora is the most destructive disease of pome fruit trees. The pathogen induces the disease by secreting HrpN, HrpW, and DspA/E effector proteins into host tissues triggering oxidative burst. To study the role of these effectors in the course of interaction with host plants, hrpN−, hrpW− and dspA/E− mutants were inoculated on two pear cultivars under in situ (greenhouse and immature fruit) and in vitro systems. In addition, the determinantal role of these effectors on host chloroplasts was studied under activated and inactivated electron cascade of chloroplasts. Results showed that the lack of HrpN and DspA/E effectors postponed the initiation of necrosis and also decreased necrosis progress rate in comparison with the wild type strain. In contrast, hrpW− had the least decline in the pathogenicity of fire blight. The comparison of chloroplast activity confirmed the role of effectors in in situ experiments and also revealed that HrpN could be the main factor for the interaction of the pathogen with host cell chloroplasts.

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