The TGA Transcription Factors from Clade II Negatively Regulate the Salicylic Acid Accumulation in Arabidopsis

• Published in: International journal of molecular sciences Vol. 23; no. 19; p. 11631
• Main Authors: Fonseca, Alejandro, Urzúa, Tomás, Jelenska, Joanna, Sbarbaro, Christopher, Seguel, Aldo, Duarte, Yorley, Greenberg, Jean T., Holuigue, Loreto, Blanco-Herrera, Francisca, Herrera-Vásquez, Ariel
• Format: Journal Article
• Language: English
• Published: Basel MDPI AG 01-10-2022; MDPI
• Subjects: Accumulation; Acids; Arabidopsis; AvrRPM1; Botanik; Botany; Chloroplasts; Gene expression; Genes; Homeostasis; Isochorismate synthase; Microbiology; Mikrobiologi; Negative feedback; Pathogens; Proteins; Pseudomonas syringae; Salicylic acid; TGA transcription factors; tga256; Transcription factors; UV-C; Virulence
• ISSN: 1422-0067; 1661-6596; 1422-0067
• DOI: 10.3390/ijms231911631

Salicylic acid (SA) is a hormone that modulates plant defenses by inducing changes in gene expression. The mechanisms that control SA accumulation are essential for understanding the defensive process. TGA transcription factors from clade II in Arabidopsis, which include the proteins TGA2, TGA5, and TGA6, are known to be key positive mediators for the transcription of genes such as PR-1 that are induced by SA application. However, unexpectedly, stress conditions that induce SA accumulation, such as infection with the avirulent pathogen P. syringae DC3000/AvrRPM1 and UV-C irradiation, result in enhanced PR-1 induction in plants lacking the clade II TGAs (tga256 plants). Increased PR-1 induction was accompanied by enhanced isochorismate synthase-dependent SA production as well as the upregulation of several genes involved in the hormone’s accumulation. In response to avirulent P. syringae, PR-1 was previously shown to be controlled by both SA-dependent and -independent pathways. Therefore, the enhanced induction of PR-1 (and other defense genes) and accumulation of SA in the tga256 mutant plants is consistent with the clade II TGA factors providing negative feedback regulation of the SA-dependent and/or -independent pathways. Together, our results indicate that the TGA transcription factors from clade II negatively control SA accumulation under stress conditions that induce the hormone production. Our study describes a mechanism involving old actors playing new roles in regulating SA homeostasis under stress.