The PTI to ETI Continuum in Phytophthora-Plant Interactions

Abstract

Phytophthora species are notorious pathogens of several economically important crop plants. Several general elicitors, commonly referred to as Pathogen-Associated Molecular Patterns (PAMPs), from Phytophthora spp. have been identified that are recognized by the plant receptors to trigger induced defense responses in a process termed PAMP-triggered Immunity (PTI). Adapted Phytophthora pathogens have evolved multiple strategies to evade PTI. They can either modify or suppress their elicitors to avoid recognition by host and modulate host defense responses by deploying hundreds of effectors, which suppress host defense and physiological processes by modulating components involved in calcium and MAPK signaling, alternative splicing, RNA interference, vesicle trafficking, cell-to-cell trafficking, proteolysis and phytohormone signaling pathways. In incompatible interactions, resistant host plants perceive effector-induced modulations through resistance proteins and activate downstream components of defense responses in a quicker and more robust manner called effector-triggered-immunity (ETI). When pathogens overcome PTI—usually through effectors in the absence of R proteins—effectors-triggered susceptibility (ETS) ensues. Qualitatively, many of the downstream defense responses overlap between PTI and ETI. In general, these multiple phases of Phytophthora-plant interactions follow the PTI-ETS-ETI paradigm, initially proposed in the zigzag model of plant immunity. However, based on several examples, in Phytophthora-plant interactions, boundaries between these phases are not distinct but are rather blended pointing to a PTI-ETI continuum.

The rise, fall and resurrection of chemical‐induced resistance agents

“…Furthermore, while it is acceptable to portray ETI, PTI and BR as different types of resistance within an evolutionary context, they are remarkably similar from a mechanistic point. All three types of resistance share similar signalling pathways and defence mechanisms that become active during different stages of the interaction with avirulent, nonhost and virulent pathogens, respectively 10,11 . These pathways and mechanisms include relatively early‐acting local defences, such as the accumulation of reactive oxygen species and cell‐wall reinforcements 12–15 .…”

“Core” RxLR effectors in phytopathogenic oomycetes: A promising way to breeding for durable resistance in plants?

“…One fascinating fact about RxLR effectors is their ability to operate as "double edge swords", where on one side they suppress host immune responses, while on the other side they act as avirulence (Avr) factors leading to R protein mediated defenses in plants [11]. Screening for potential R proteins that recognize Avr RxLR effectors of oomycetes has been attempted [95,[137][138][139][140][141].…”

“…Undisputedly, deployment of R-genes is the most effective, environmentally sound, and widely used strategy for providing disease resistance to crop plants. Although this approach has been actively used for over a century, it is unfortunate that some R-genes [30] Suppress pattern-triggered immunity and some induce hypersensitive responses [78] Hyaloperonospora arabidopsidis 18 [4] RXLR29 was shown to suppress pathogen-induced callose deposition [153] Bacteria Ralstonia solanacearum 60-75 [32] - [154][155][156] Xanthomonas arboricola 57 [11] - [157] Fungi Ustilaginoidea virens 193 [18] UV_1261 suppress host plant hypersensitive responses [158][159][160] Zymoseptoria tritici 591 [153] - [161] Ustilago maydis 467 (202) Pep1 inhibits the activity of the apoplastic maize peroxidase POX12 Cce1 hypothesized to inhibit early plant defense responses in the apoplast Rsp3 has a conserved virulence role of protecting the fungal hyphae from maize antifungal proteins activity. Sta1 a novel core effector with virulence role through host cell-wall modification for disease progression [27,[162][163][164][165][166][167] Colletotrichum orbiculare necrosis-inducing secreted protein 1 (NIS1), targets conserved immune kinases hence interfering with PTI signaling [115] have been overpowered in a single season due to the evolution of new virulence traits within pathogen populations (resistance-breaking strains) [15,16].…”

Enhancing Our Understanding of Plant Cell-to-Cell Interactions Using Single-Cell Omics

“…Upon recognition of the pathogen, a first response, the MAMP-triggered immunity response, is initiated. Later, the effector-triggered immunity response will allow the infected plant cell to initiate a more specific response to the microbe (Jones and Dangl, 2006;Naveed et al, 2020). These two types of immunity form the plant cellautonomous immunity.…”