Biological Functions of Arabidopsis TGA1 and TGA4 Transcription Factors

Abstract

Plant immune system comprises three main layers. Recognition of conserved microbe-associated molecular patterns (MAMPs) initiates the first layer of immune response, known as MAMP-triggered immunity (MTI). However successful pathogens utilize virulent strategies, such as effector proteins, to suppress MTI and facilitate their growth, resulting into effector-triggered susceptibility (ETS). In response to ETS, plants acquire resistance proteins (R proteins) to monitor the presence of the pathogen effector proteins, leading to stronger immune response, known as effector-triggered immunity (ETI). During the plant immune response, large-scale transcriptional reprogramming is activated by numerous transcription (co)factors. The Arabidopsis TGA factors have been shown to be required for resistance to disease. In the present study, the biological functions of clade I TGA factors (TGA1 and TGA4) during plant immune responses were investigated in depth. My results demonstrate that the Arabidopsis TGA1 and TGA4 are positive regulators in disease resistance against various types of pathogens. Multiple mutant alleles and overexpression lines of clade I TGA factors were identified and analyzed to confirm the previous finding that clade I TGA factors positively contribute to ETS against a virulent race of the bacterial pathogen Pseudomonas syringae and further discover their positive role in ETS against the fungal pathogen Colletotrichum higginsianum. In addition, clade I TGA factors were shown to play important roles in MTI-mediated disease resistance against P. syringae pv. tomato hrcC-, and ETI-mediated disease resistance against P.s.t. AvrRpt2. Furthermore, clade I TGA factors are required for non-host resistance against P. syringae pv. phaseolicola 1448a, wich relies on both MTI and ETI. Loss of resistance in mutants of clade I TGA factors was shown to be associated with defects in cell wall-based defence responses, including callose deposition, apoplastic oxidative burst and extracellular PR-1 protein accumulation. Interestingly, transcript levels of PR-1, callose synthase and other genes encoding defence proteins accumulated at, or above, wild type levels in the mutants. Furthermore, the double mutant is more sensitive to the glycosilation inhibitor, tunicamycin, indicative of a compromised endoplasmic reticulum (ER) stress response. These results suggest that clade I TGA factors control defence-related secretion events that are required for cell wall-associated defence responses. Analysis of the non-expressor of pathogenesis-related genes 1 (npr1-1) mutant and an tga1-1 tga4-1 npr1-1 triple mutant indicate that clade I TGA factors act substantially independent of NPR1 during plant immune responses. Moreover, mutation of clade I TGA factors also results in developmental changes, including curly leaves and late flowering. Together, these results demonstrate that TGA1 and TGA4 factors play a unique role in mediating both defence responses and developmental processes.