# Regulation of the _Pseudomonas syringae_ Type III Secretion System by Host Environment Signals
### The P. syringae Type III Secretion System (T3 SS) and Its Role in Virulence  
_P. syringae_ rely on a type III secretion system (T3 SS) to cause disease in host plants [12; 13]. The T3 SS is a syringe-like translocon comprised of a barrel-like basal body that spans both bacterial cell membranes, and an extracellular filament termed the pilus [14; 15]. The T3 SS pilus extends through the plant cell wall and likely makes direct contact with the host plasma membrane, forming a continuous channel between the bacterium and host cell. While the T3 SS is a common feature among both plant and animal pathogens, plant pathogens including _P. syringae_ produce a T3 SS pilus that is significantly longer than those typically produced by animal pathogens, presumably in order to breach the thick barrier of the plant cell wall [14; 16].  
During host infection, a subset of bacterial proteins, collectively termed T3 SS effectors, are trafficked through the hollow inner channel of the T3 SS and delivered directly into the host cytosol. Following their translocation into the host cell, many T3 SS effectors inhibit various facets of host immune signaling, effectively suppressing the host defense response [17]. _P. syringae_ pathways typically possess a repertoire of >20 different effectors, which carry out various functions within the plant host [18; 19; 20; 21]. Some T3 SS effectors directly interact with and disrupt the function of plant cell-surface receptors and/or co-receptors that are involved in the immune detection of microbial invaders [22; 23; 24]. Furthermore, numerous _P. syringae_ T3 SS effectors interrupt various stages of the host signaling cascade initiated by these immune receptors, and/or curtail the deployment of immune-triggered antimicrobial defenses [25; 26; 27; 28]. Other T3 SS effectors promote pathogen entry into the apoplast by regulating stomatal aperture, through interaction with plant immune regulators such as RIN4 or the modulation of the plant hormone jasmonic acid [29; 30; 31]. Additionally, T3 SS effectors can promote _P. syringae_ fitness in the apoplast by stimulating water release from host cells [32].  
Most T3 SS effectors contribute redundantly to disarming host immunity and are individually dispensable for virulence. However, individual genes encoding the T3 SS translocon itself are required for _P. syringae_ to effectively colonize host tissues [12; 33; 34]. Similarly, while the T3 SS effector repertoire varies substantially across different _P. syringae_ pathways, core components of the T3 SS are highly conserved throughout Gram-negative bacteria [34; 35]. Genetic loci encoding the T3 SS were thus designated as _hrp_ (_luppersensitive response and pathogenicity_) and/or _lrc_ (_luppersensitive response and conserved_) genes, which are organized into the conserved _hrp_/_lrc_ pathogenicity cluster (Figure 1A). While many genes within the _lrp_/_lrc_ cluster are required for _P. syringae_ virulence, the specific function of several of these virulence factors remains ambiguous [36; 37]. For example, the regulatory gene _hrp_T encodes a putative lipoprotein required for T3 SS production and virulence by _P. syringae_, yet its function has not been fully determined [36; 37; 38]. The _hrp_/_lrc_ cluster is located within the tripartite pathogenicity island (T-PAI), along with two loci encoding the majority of T3 SS effectors [34]. The canonical T-PAI is present in most lineages within the _P. syringae_ species complex, and is thought to be the result of horizontal gene acquisition by an ancestral strain similar to the non-pathogenic soil bacteria _Pseudomonas fluorescens_[17; 39]. Additionally, many T3 SS effector genes are located outside of the T-PAI throughout the _P. syringae_ genome [40].