Abstract
Even though resistance (R) genes are among the most studied components of the plant immunity, there remain still a lot of aspects to be explained about the regulation of their function. Many gain-of-function mutants of R genes and loss-of-function of their regulators often demonstrate up-regulated defense responses in combination with dwarf stature and/or spontaneous leaf lesions formation. For most of these mutants, phenotypes are a consequence of an ectopic activation of R genes. Based on the compilation and comparison of published results in this field, we have concluded that the constitutively activated defense phenotypes recurrently arise by disruption of tight, constitutive and multilevel negative control of some of R proteins that might involve also their targeting to the autophagy pathway. This mode of R protein regulation is supported also by protein–protein interactions listed in available databases, as well as in silico search for autophagy machinery interacting motifs. The suggested model could resolve some explanatory discrepancies found in the studies of the immunity responses of autophagy mutants.
Highlights
There are several approaches how to study and classify the plant immunity related events, and the most widespread is division of the plant immunity into two modes – a pathogen-associated molecular patterns (PAMPs) triggered immunity (PTI), which is triggered usually by recognition of structural components of pathogen on the surface of the host cell, and effector triggered immunity (ETI; Jones and Dangl, 2006)
ETI is triggered by the direct or indirect interaction between a specific disease resistance (R) protein and a corresponding avirulence (Avr) protein of pathogen and is accompanied by a number of changes within the plant – production of reactive oxygen species (ROS) by an oxidative burst, accumulation of the salicylic acid (SA), and the transcriptional activation of genes involved in defense response, that lead to a possible final stage – localized programmed cell death called the hypersensitive response (HR; Pontier et al, 1998; review in McDowell and Woffenden, 2003; Vlot et al, 2008)
HR cell death triggered by R proteins RPS4, RPP1 and RPM1 was significantly suppressed in atg mutants; especially the first two of them which signal through ENHANCED DISEASE SENSITIVITY 1 (EDS1) signaling component
Summary
There are several approaches how to study and classify the plant immunity related events, and the most widespread is division of the plant immunity into two modes – a pathogen-associated molecular patterns (PAMPs) triggered immunity (PTI), which is triggered usually by recognition of structural components of pathogen on the surface of the host cell, and effector triggered immunity (ETI; Jones and Dangl, 2006). In plants overexpressing a CNL gene ACTIVATED DISEASE RESISTANCE 1 (ADR1), a constitutive defense response and a dwarf phenotype were found (Grant et al, 2003).
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
