AI Article Synopsis
- Oomycete pathogens use crinkling and necrosis proteins (CRNs) to manipulate plant defenses, but how these proteins work is not fully understood.
- The study focuses on the effector PsCRN108, which not only inhibits the expression of certain immune-related genes but also interacts with a key regulatory protein, NbCAMTA2, enhancing its inhibitory effect on plant immunity.
- The findings reveal that PsCRN108 can suppress plant immunity through complex interactions with transcription factors, outlining a new mechanism of how CRN effectors function in pathogenicity.
Article Abstract
Oomycete pathogens secrete numerous crinkling and necrosis proteins (CRNs) to manipulate plant immunity and promote infection. However, the functional mechanism of CRN effectors is still poorly understood. Previous research has shown that the effector PsCRN108 binds to the promoter of s and inhibits their expression, resulting in impaired plant immunity. In this study, we found that in addition to , PsCRN108 also suppressed other () family genes, including . Interestingly, PsCRN108 inhibited the expression of through its promoter, but did not directly bind to its promoter. Instead, PsCRN108 interacted with NbCAMTA2, a negative regulator of plant immunity. NbCAMTA2 was a negative regulator of expression, and PsCRN108 could promote such inhibition activity of NbCAMTA2. Our results elucidated the multiple roles of PsCRN108 in the suppression of plant immunity and revealed a new mechanism by which the CRN effector hijacked transcription factors to affect immunity. [Formula: see text] Copyright © 2024 The Author(s). This is an open access article distributed under the CC BY-NC-ND 4.0 International license.
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| http://dx.doi.org/10.1094/MPMI-05-23-0058-R | DOI Listing |
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