Secretory Peptides as Bullets: Effector Peptides from Pathogens against Antimicrobial Peptides from Soybean

Abstract

Soybean is an important crop as both human food and animal feed. However, the yield of soybean is heavily impacted by biotic stresses including insect attack and pathogen infection. Insect bites usually make the plants vulnerable to pathogen infection, which causes diseases. Fungi, oomycetes, bacteria, viruses, and nematodes are major soybean pathogens. The infection by pathogens and the defenses mounted by soybean are an interactive and dynamic process. Using fungi, oomycetes, and bacteria as examples, we will discuss the recognition of pathogens by soybean at the molecular level. In this review, we will discuss both the secretory peptides for soybean plant infection and those for pathogen inhibition. Pathogenic secretory peptides and peptides secreted by soybean and its associated microbes will be included. We will also explore the possible use of externally applied antimicrobial peptides identical to those secreted by soybean and its associated microbes as biopesticides.

Keywords: antimicrobial; biopesticide; effector; endophyte; pathogen; rhizospheric microbe; secretory peptide; signaling; soybean.

Figure 1

The overview of plant defense response. The interplay between pathogens, PTI (PAMP-triggered immunity), and ETI (effector-triggered immunity) is illustrated by the classic zig-zag model [79]. PAMPs (pathogen-associated molecular patterns) are recognized by PRRs (pathogen recognition receptors) and trigger the defense responses of plants. Some pathogens have developed effectors to neutralize PTI in plants. Consequently, plants develop ETI to counter the effects of pathogen effectors, and ETI is known as a boosted PTI response. ETI then triggers the onset of HR (hypersensitive response), in which ROS are produced to disrupt cell membrane, thicken the cell wall, induce JA (jasmonic acid) and SA (salicylic acid) production, and eventually, PCD (programmed cell death). The production of ROS also triggers the onset of SAR (systemic acquired resistance) to render the resistance to a broad spectrum of pathogens.

Figure 2

Representation of a selection of recently reported virulence peptides involved in the infection of plant cells by P. sojae. This figure shows a snapshot of the widespread metabolic changes induced by this oomycete as a result of the infection. (0) The haustorium penetrates soybean tissues and secretes effector peptides close to and into the plant cells [44]. (1) PsAvh23 binds to the regulatory subunit of the H3K9 histone acetyltransferase (HAT), preventing it from associating with the catalytic subunit and therefore, suppressing defense gene activation [15]. (2) PsAvh52 translocates the putative transacetylase protein GmTAP1 to the nucleus, leading to the acetylation of core histones and the upregulation of plant susceptibility genes [115]. (3) PsAvr3c stabilizes the spliceosome-associated protein GmSKRP1/2, causing changes in host pre-mRNA splicing, thus impairing plant immunity [117]. (4) PsAvh238 interacts with a type-2 aminocyclopropane-1-carboxylate synthase (GmACS), a key enzyme in ethylene biosynthesis, which disrupts ethylene signaling and therefore, impairs pathogen-induced stress responses in the plant host [120]. (5) PsAvh262 suppresses ER stress-triggered cell death by stabilizing luminal binding immunoglobulin proteins (BiPs), and therefore, promoting infection [121].

Figure 3

The secretion mechanism and modes of action of nodule-specific cysteine-rich (NCR) peptides. NCR peptides secreted at 4–7 days post inoculation (dpi) with rhizobia and at 10–14 dpi are classified as early and late NCR peptides, respectively [145]. The host root cells recognize unknown signals from the rhizobia and secrete NCR peptides, which may selectively inhibit incompatible rhizobia [139] and mediate bacteroid formation [137,138].