The major leaf ferredoxin Fd2 regulates plant innate immunity in Arabidopsis

Abstract

Ferredoxins, the major distributors for electrons to various acceptor systems in plastids, contribute to redox regulation and antioxidant defence in plants. However, their function in plant immunity is not fully understood. In this study, we show that the expression of the major leaf ferredoxin gene Fd2 is suppressed by Pseudomonas syringae pv. tomato (Pst) DC3000 infection, and that knockout of Fd2 (Fd2-KO) in Arabidopsis increases the plant's susceptibility to both Pst DC3000 and Golovinomyces cichoracearum. On Pst DC3000 infection, the Fd2-KO mutant accumulates increased levels of jasmonic acid and displays compromised salicylic acid-related immune responses. Fd2-KO also shows defects in the accumulation of reactive oxygen species induced by pathogen-associated molecular pattern-triggered immunity. However, Fd2-KO shows enhanced R-protein-mediated resistance to Pst DC3000/AvrRpt2 infection, suggesting that Fd2 plays a negative role in effector-triggered immunity. Furthermore, Fd2 interacts with FIBRILLIN4 (FIB4), a harpin-binding protein localized in chloroplasts. Interestingly, Fd2, but not FIB4, localizes to stromules that extend from chloroplasts. Taken together, our results demonstrate that Fd2 plays an important role in plant immunity.

Chloroplasts and Plant Immunity: Where Are the Fungal Effectors?

“…This hormone imbalance induced JA-dependent defense gene expression and further led to reduced expression of SA biosynthetic genes (e.g., ICS1) and SA-dependent genes (e.g., PR1). In ETI with P. syringae containing avrRpt2, plants lacking flavodoxin produced~2 times more H 2 O 2 and consequently were more resistant than wild-type plants [39]. Ferredoxin2 was found to be located in stromules, which indicates a potential contribution to retrograde signaling [39].…”

“…In ETI with P. syringae containing avrRpt2, plants lacking flavodoxin produced~2 times more H 2 O 2 and consequently were more resistant than wild-type plants [39]. Ferredoxin2 was found to be located in stromules, which indicates a potential contribution to retrograde signaling [39].…”

“…The WKS1 protein is located in the chloroplast, and was shown to interact with and ultimately phosphorylate a thylakoid-associated ascorbate peroxidase, thus limiting ascorbate detoxification of ROS leading to a slow cell death response and partial plant resistance [38]. The impact of ROS in the defense against hemibiotrophs is illustrated by an analysis of Arabidopsis plants expressing a ferrodoxin that is a major distributor of electrons in plastids [39]. Deletion of the gene encoding the plastid-localized ferredoxin FD2 led to increased virulence of the bacterial pathogen P. syringae, and this was correlated with a reduction in ROS formation during PTI [39].…”

“…The impact of ROS in the defense against hemibiotrophs is illustrated by an analysis of Arabidopsis plants expressing a ferrodoxin that is a major distributor of electrons in plastids [39]. Deletion of the gene encoding the plastid-localized ferredoxin FD2 led to increased virulence of the bacterial pathogen P. syringae, and this was correlated with a reduction in ROS formation during PTI [39]. Plants lacking FD2 showed dramatically induced JA formation, while SA formation was unchanged compared to wild type plants.…”

Oxathiapiprolin, a Novel Chemical Inducer Activates the Plant Disease Resistance

“…Plant hormones were extracted and detected according to the previous reports [59,60]. In brief, the mock or OX-treated Arabidopsis plants were infiltrated with buffer (10 mM MgCl 2 ) or buffer containing the Pst DC3000 cells.…”