Biotic Stress/Applied Plant Bio

Abstract

CS-23-3 - Translation Regulator GCN2 controls ABA Homeostasis and Stomatal Immunity in Arabidopsis

Tuesday, July 17
9:13 AM - 9:33 AM

Upon pathogen challenge, plants rapidly redirect cellular resources from growth to defense by inducing defense-related gene expression, either at transcriptional or translational level. General Control Non-derepressible 2 (GCN2) is an evolutionarily conserved serine/threonine protein kinase that plays an essential role in modulating amino acid metabolism in response to nutrient deprivation in yeast, human and other eukaryotes. GCN2 binds to uncharged tRNAs, leading to phosphorylation of eukaryotic Initiation Factor 2a. These events trigger a global translational repression but stimulate translation of selective mRNAs that contain upstream open reading frames. Here, we demonstrate that in Arabidopsis, bacterial infection activates the AtGCN2-eIF2a pathway, which consequently reinitiates the translation of a defense-related transcription factor TBF1. We discovered that AtGCN2 regulates a subset of ABA signaling components through TBF1-dependent transcription. While the roles of ABA in pre-invasive and post-invasive defenses have been proposed, it remains to be determined how virulent bacterial pathogens might manipulate this phytohormone to induce effective defenses or establish host susceptibility during pathogen infection. Here, we provide a missing link describing how GCN2 fine-tunes the accumulation of ABA and ABA-mediated signaling players during the pre-invasive and post-invasive stages of an infection event. Finally, we also show that AtGCN2 is required for the perception of phytotoxin coronatine secreted by P. syringae. During the pre-invasive stage, AtGCN2 regulates stomatal immunity by affecting the pathogen-triggered stomatal closure and coronatine-mediated stomatal reopening. Our conclusions suggest a conserved and ancient role of GCN2 in various forms of immune responses across kingdoms, highlighting AtGCN2 as a molecule of key interest in studies on both plant and mammalian immunology.


 

Co-Authors

Xiaoyu Liu – University of Alabama at Birmingham

Karolina M. Mukhtar, PhD

Associate Professor
University of Alabama at Birmingham

Dr. Karolina Mukhtar is an Associate Professor of Biology at the University of Alabama at Birmingham. She obtained her PhD in the IMPRS doctoral program at the Max Planck Institute in Cologne, Germany (2002-2005). Her dissertation described the quantitative basis of plant resistance to P. infestans and P. carotovorum. Subsequently Karolina conducted post-doc research in the laboratory of Dr. Xinnian Dong at Duke University (2006-2010). This work uncovered the existence of a previously unknown transcriptional growth-to-defense molecular switch in plants.
Karolina joined UAB in 2010 as Assistant Professor, and was tenured and promoted to Associate Professor in 2016. She also serves as Associate Chair of the UAB Biology Department. Research in Karolina’s lab focuses on ER stress, Unfolded Protein Response and translational regulation of immune responses. Work in Karolina’s lab is funded by NSF-CAREER award.

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