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Phytophthora hijacks host BAG7 and bZIP28 resulting in sequestration in endoplasmic reticulum for compatibility via effector-mediated BiP accumulation
Maofeng Jing: Texas A&M University; Yurong Li: Texas A&M University; Yuanchao Wang: Nanjing Agric Univ; Martin Dickman: Texas A&M University
<div>The endoplasmic reticulum (ER) is a central hub for stress responses to pathogens as well environmental<i> </i><i>Phytophthora</i> species secrete a large array of specific effector proteins to manipulate host innate immunity.<i> Phytophthora </i>uses an essential effector, Avh262 to stabilize Binding immunoglobulin Proteins (BiPs) in the ER, that act as negative regulators of plant resistance to <i>Phytophthora</i> and ER stress-induced cell death (ERCD), can result in attenuated plant defense responses. However, little is known about how <i>Phytophthora</i> hijack the host BiPs to regulate the ER machinery for successful infection. Here we show Avh262 interacts with both AtBAG7, an ER-localized cochaperone that helps maintain for the maintenance of the unfolded protein response, and bZIP28, an ER membrane-tethered transcription factor. The translocation of AtBAG7 and bZIP28 from the ER to the nucleus is required for activating the downstream pathways. We found AtBAG7 negatively regulates plant resistance to <i>Phytophthora</i>, and bZIP28 plays a positive role. The culture filtrate of <i>Phytophthora</i><i> </i>triggers the translocation of AtBAG7 and bZIP28 from the ER to the nucleus, which can be prevented by the Avh262-mediated accumulation of BiPs. In conclusion, <i>Phytophthora</i> pathogens secrete effectors to accumulate high level of BiPs, which retains AtBAG7 and bZIP28 in the ER lumen, resulting in suppressing the ERCD pathway and blocking expression of downstream defense genes, beneficial to infection.</div>

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