Effector-triggered post-translational modifications and their role in suppression of plant immunity

Abstract

Plant-pathogen interactions feature complex signaling exchanges between host and microbes that ultimately determine association outcomes. Plants deploy pattern recognition receptors to perceive pathogen-associated molecular patterns, mount pattern-triggered immunity (PTI), and fend off potential pathogens. In recent years an increasing number of defense-signaling components have been identified along with a mechanistic understanding of their regulation during immune responses. Post-translational modifications (PTMs) are now thought to play a crucial role in regulating defense signaling. In a bid to suppress PTI and infect their host, pathogens have evolved large repertoires of effectors that trigger susceptibility and allow colonization of host tissues. While great progress has been made in elucidating defense-signaling networks in plants and the activities of effectors in immune suppression, a critical gap exists in our understanding of effector mechanism-of-action. Given the importance of PTMs in the regulation of defense signaling, we will explore the question: how do effectors modify the post-translational status of host proteins and thus interfere with host processes required for immunity? We will consider how emerging proteomics-based experimental strategies may help us answer this important question and ultimately open the pathogens' effector black box.

Keywords: PAMP-triggered immunity; direct effector-triggered modification; effector; effector-triggered susceptibility; indirect effector-triggered modification; post-translational modifications.

FIGURE 1

(A,B) Modulation of host defense-signaling networks by pathogen effectors. One example of effector mediated host defense modulation is the manipulation of mitogen-activated protein kinase (MAPK) phosphorylation cascades. (A) Host defenses may be activated by the perception and binding of pathogen-associated molecular patterns (PAMPs) by host pattern recognition receptors (PRRs) with the aid of a co-receptor (CR). Successful PAMP perception triggers a MAPK phosphorylation cascade resulting in transcription factor (TF) activation, defense gene expression and PAMP-triggered immunity (PTI). However, pathogen effectors (E) can manipulate this signaling pathway at a number of key steps (B) resulting in effector-triggered susceptibility (ETS). For example, the MAPK cascade can be blocked either by the effector perturbing CR-PRR activities or by the effector modifying MAPKs directly. Alternatively, nuclear targeting effectors may block defense gene induction, ultimately leading to enhanced susceptibility and the onset of disease. (C) Two models for effector-triggered post-translational modifications. In Model 1 (direct effector-triggered modification – DETM) the effector (E) binds the host target protein (T) and directly catalyzes its post-translational modification (PTM). In Model 2 (indirect effector-triggered modification – IETM) the effector binds the target protein and recruits a host machinery (HM) which catalyzes target PTM. The modified host protein may then be subject to proteasome mediated degradation (1), altered structural confirmation and activity (2), or re-localization (3).