4.  Structural defence/Physical barriers

Plants use physical barriers as a borderline of defence strategy. Unlike animals, plants have developed a ravishing array of physical, chemical and protein-based defences for detection of assaulting organisms and protection against severe damage. The simplest mechanisms are pre-existing passive resistance barriers like waxy cuticular surfaces, rigid cell walls and a variety of antimicrobial compounds. Pathogens need to subvert these barriers as the first tier of defence installed by the plants. The cuticular surface consists of a waxen layer on top of epidermal cells that covers the plant tissue for safeguarding the host from many pathogens. However, some physiological entry sites like stomata, hydathodes or wound points are unavoidably present in plants, which allow pathogens easy access. Once inside, the invading pathogens confront an adverse environment such as unfavorable pH, antimicrobial compounds and even thick cell walls before reaching host cellular contents.

Even after overcoming such obstacles, an invading pathogen faces the molecular weapons of plant innate immunity. Most pathogens have evolved the capacity to penetrate the passive barriers and enter the intracellular space of the plants but in turn, plants have evolved more sophisticated and specialized defensive strategies to perceive and prevent such assaults.

{Need to collect and add more examples, such as:

Moreover, the cuticle, rigid epidermal cell wall etc. work as structural defence/physical barriers to defend the pathogenic attack}

5.  Plant innate immunity

Plants are not defenceless against pathogenic attack, and host genotypes possess resistance (R) genes, the products of which have evolved the capacity to recognize specific effector molecules and activate a disease resistance response (Figure 1.2). R proteins recognize and interact with effector proteins, activating ETI. This response culminates in the death of the infected cell, which effectively starves the pathogen of nutrients, preventing colonization and disease symptoms. The host is thus forfeiting a few cells to maintain a competitive advantage for the whole plant to ensure flowering and fruit setting. Also, host plants deploy a two-layered innate immune system incorporating both plasma membrane-associated and cytoplasmic immune responses.

Two-layered innate immune system

 MAMP- or PAMP-triggered immunity /perception/sense of microbes through PRRs.

The primary immune strategy is referred to as microbe or pathogen associated molecular pattern (MAMP/PAMP)-triggered immunity (PTI), by which the common features (MAMP or PAMP) of microbial invaders are detected, and a basal resistance response is triggered. This immune strategy is coined as MAMP/PAMP- triggered immunity (PTI). In this case, PAMP recognition receptors (PRRs) detect the macromolecules (MAMP/PAMP) usually within the extracellular spaces of the host plants. Apparently, a threshold level of PAMP (e.g., flagellin) needs to come in contact with host surfaces for activation of a PTI response. This pathway involves the recognition of conserved pathogen molecules (PAMPs), by receptors positioned at plant cell surfaces named as transmembrane PRRs. A well characterised feature of PTI is the recognition of bacterial flagellin by the PRRs in both plant and animal systems. Recognition of a PAMP by the PRRs stimulates a signalling cascade involving Mitogen- Activated Protein Kinases (MAPK) and Ca2+ fluxes. This leads to a set of defensive maneuvers such as induction of reactive oxygen species (ROS), cell alkalinisation and accumulation of callose in the cell walls, for restricting pathogen permeation. However, most pathogens have evolved competence to evade such maneuvers by deploying effector molecules in the cells. Furthermore, the secreted effectors can in some cases coerce the physiology of the host cell into service of the invading pathogen.

Effector-triggered immunity (ETI)

One much-studied plant-pathogen interaction is Effector-Triggered Immunity (ETI), in which the plant resistance machinery detects and interacts with the effector proteins secreted by the pathogen. Key components of host plant immunity are resistance genes (R) that encode receptor-like proteins capable of recognizing specific pathogenic effector molecules. Upon recognition of avirulence (Avr) effectors, the R protein switches on a defence response characterized by rapid induced necrotic cell death at the infection site, which restricts the further growth and spread of the pathogens.

The interactions between the effector proteins and the cognate R proteins underlie gene-or-gene specificity and coevolution of pathogenic avirulence genes and plant resistance genes. In the co-evolution of host-microbe interactions, pathogens evolved effector proteins secreted into the plant cells, the role of some being to deceive PTI and thus favour pathogen growth and disease. To confront such pathogenic manoeuvres, host plants advanced a second layer of immune strategy by recognizing the effectors with proteins known as R proteins, which leads defence responses towards

microbial invaders that have acclimatized to elude PTI. In this case, the pathogens are identified by the plants through detection of specialized effector molecules delivered by the pathogens at the onset of infection process. The genetic basis of ETI has been designated as the “Gene-for-Gene” concept (Flor, 1971),  where every R gene has a corresponding pathogenic gene capable of conferring pathogenicity for the pathogen, which is in most cases an effector. Recognition of the effector proteins appears to occur in the cytoplasm, either by the direct or indirect interaction between the individual effector and its cognate R protein. In contrast to PTI, ETI culminates in a hypersensitive response (HR) leading to programmed cell death (PCD) at the sites of infection.

2. Effector proteins - weapons to facilitate pathogenicity

Effectors  are  small  protein  molecules  secreted  by  pathogens  into  host  plant  to promote infection through manipulating host metabolism and other physiological processes to favour pathogenic survival. The pathogen delivers effectors whose collective function is to blockade the detection mechanism of the host defence system and to boost up pathogenicity  by facilitating nutrient flow from the host plant cells. Though the host plants have resistance proteins (R) as part of innate immunity, it renders race-specific resistance through recognition of pathogenic effectors. However, there are many effectors secreted by a diverse range of pathogens. A better knowledge of pathogen effectors can assist biotechnologists in understanding the functions of the R proteins and facilitate the development of resistant plants that can ensure food security. When a particular R protein recognizes an individual effector molecule, is termed an avirulence (Avr) effector with respect to that R protein, whereas those that are not recognized are known as virulence effectors (avr). Much research has been carried out on the general aspects of pathogen effectors, showing that for successful biotrophic infection in a plant, pathogens must first bypass plant basal defence and then overcome plant innate immunity either by modifying host cell structure and/or function. It has been advocated that avoidance of host resistance has become possible by the deployment of effector proteins secreted by the pathogen.

Effectors are an important aspect of plant disease resistance research, and breeders are embracing such research for accelerating and improving resistance genes intending to identify, characterize and deploy in their breeding programs.