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. 2009 Jun 30;7(6):e1000139. doi: 10.1371/journal.pbio.1000139

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Liu et al.

This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.

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RIN4 acts in concert with AHA1 and/or AHA2 to regulate stomatal apertures in response to pathogen attack during PTI. (A) Virulent pathogens are able to overcome PTI and induce stomata to re-open 3 h after pathogen perception. Activation of the PM H⁺-ATPase can lead to hyperpolarization of the plasma membrane and subsequent induction of inward K⁺ channels. These events lead to an increase in guard cell turgor and stomatal opening. (B) RIN4 is a negative regulator of plant innate immunity. In resistant genotypes, pathogens are not able to overcome PTI and stomata remain closed after pathogen perception. Pathogen PAMPs are detected by pattern recognition receptors (PRRs) and the induction of PTI induces stomatal closure. Posttranslational modification of RIN4 (elimination or possibly phosphorylation) inhibits the association between RIN4 and AHA1/AHA2, resulting in inactivation of the PM H⁺-ATPase.