SUMMARY OF CELL TO CELL COMMUNICATION

 Plant cells use plasmodesmata and the apoplast to communicate with

each other during defense responses against pathogens.
 Pathogen recognition activates signaling pathways like MAPK, ROS,
Ca2+ along with hormone signaling to execute defense responses
locally and systemically.
 Pathogens can manipulate plant cellular and hormone signaling and
exploit plasmodesmata and intercellular connections to infect hosts.
 Plants have constitutive and induced defenses. Induced defenses include
PTI, ETI, and SAR activated by PAMP and effector recognition.
 Effectors can suppress PTI by interfering with signaling pathways and
plasmodesmata to promote Effector-Triggered Susceptibility.
 Resistance proteins can recognize effectors and trigger ETI responses
like HR cell death to restrict pathogen spread.
 Hormones like SA, JA, and auxin play roles in both development and
immunity partly by regulating plasmodesmata permeability.
 Pathogens like viruses, fungi, nematodes exploit plasmodesmata and
movement of effectors to infect neighboring cells.
 Long-distance defense signals like SA, RNAs, peptides move through
plasmodesmata and vasculature to activate systemic defenses.
 Future studies on multi-omics integration can help understand how
pathogens manipulate intercellular communication for infection.

 Plants have apoplastic and symplastic routes for cell-to-cell

communication mediated by plasmodesmata and the apoplast space.
 Basal defenses include physical barriers like the cuticle and cell wall, and
chemical defenses like antimicrobial compounds.
 PAMP-triggered immunity (PTI) is activated upon pattern recognition
receptor detection of PAMPs and induces responses like MAPK
activation and calcium signaling.
 Effectors delivered by pathogens can suppress PTI, causing effector-
triggered susceptibility (ETS). Some effectors move cell-to-cell.
  Effector recognition by resistance proteins triggers effector-triggered
immunity (ETI) and hypersensitive response cell death.
 Systemic acquired resistance (SAR) is activated through mobile signaling
molecules that induce distal defenses.
 Hormones like SA, JA and auxin regulate defenses and plasmodesmata
permeability. Pathogens manipulate hormone pathways.
 Nematodes form feeding sites through the apoplast. Viruses hijack
plasmodesmata trafficking using movement proteins.
 Fungi can enter via wounds or natural openings and spread
symplastically. Some fungal effectors also move cell-to-cell.
 Bacteria generally colonize through the apoplast but can also deliver
effectors intracellularly.

SYMPLASTIC COMMUNICATION

 Plants have evolved plasmodesmata (PDs) to enable symplastic

communication between cells, allowing transport and signaling through
the rigid cell wall.
 PDs are pores lined by plasma membrane and contain endoplasmic
reticulum structures like the desmotubule. Their composition is different
from the rest of the plasma membrane.
 PDs facilitate trafficking of nutrients, hormones, signaling molecules,
RNA and non-cell autonomous proteins between plant cells and organs.
 In shoot meristems, the WUS transcription factor moves through PDs
from organizing center cells to maintain stem cell fate.
 In roots, the SHR protein moves from stele to endodermis via PDs to
control cell division and fate.
 Protein passage through PDs is regulated by callose deposition at the
orifice, controlled by proteins like PDLPs and callose
synthases/glucanases.
 Callose levels and thus PD permeability also correlate with reactive
oxygen species levels and organelle redox states.
 Preformed defense
 As a first line of defense, plants use physical barriers like the cuticle, cell
wall, and Casparian strips to restrict pathogen spread between cells via
the apoplast.
 The cell wall is made of components like cutin, lignin, cellulose and
pectin. Mutants defective in these are more susceptible to pathogens.
 A second level involves constitutive secondary metabolites like
antimicrobial proteins, defensins, saponins and glucosinolates
(phytoanticipins).
 When pathogens breach the cell wall via enzymes, damage cues like
ROS and molecules can signal to neighboring cells.
 This priming induces the de novo synthesis of phytoalexins like
camalexin in neighboring cells. These can inhibit pathogen growth and
maturation.
 Plants also secrete apoplastic proteases to suppress bacteria via low pH
maintenance.
 Together these preformed and primed responses constitute apoplast
immunity at the plant-pathogen interface.

INDUCED DEFENSE

 When pathogens breach preformed defenses and reach the apoplast,

plants activate a third level of inducible defense.
 This follows the zig-zag model of pathogenesis with 3 successive steps:
1. PAMP-Triggered Immunity (PTI):
 Plants recognize pathogen-associated molecular patterns (PAMPs) via
pattern recognition receptors.
 This induces signaling pathways like MAPK, calcium, defense genes for
PTI responses.
2. Effector-Triggered Susceptibility (ETS):
 Some pathogens deliver effectors to suppress PTI via MAPK/calcium
inhibition or other mechanisms.
 3. Effector-Triggered Immunity (ETI):
 Resistant plants recognize effectors via resistance proteins to induce
faster and stronger immune responses like hypersensitive response cell
death.
 This third inducible defense level involves sophisticated molecular
recognition and signaling between the plant and pathogen as they
engage in counter-defense evolution.

PTI

 Plants recognize PAMPs like flagellin peptide flg22 via membrane-

bound pattern recognition receptors like FLS2/BAK1.
 This induces complex signaling pathways - MAPK, Ca2+, ROS, hormone
pathways and transcriptional changes.
 Some defenses occur through the apoplast like ROS, nutrient restriction,
antimicrobial compound production.
 MPK3/6 phosphorylation of WRKY33 regulates camalexin production.
 A hallmark is regulation of symplastic trafficking via callose-mediated
PD closure. Lower callose correlates with higher infection.
 Chitin is perceived by LYM2 at PDs to trigger closure via ROS/calcium
signaling involving NADPH oxidase and CPKs.
 PDs integrate calcium and ROS signaling in PTI response, though degree
varies - roots show spatial/zonal responses.
 Laser ablation studies suggest PD integrity collapse perception induces
stele response.
 ROS decreases PD permeability likely by regulating callose deposition,
but mechanisms are unknown.
 PDLP1/5 may function with DUF26 ROS sensor to mediate PAMP-
triggered ROS signal at PDs.
ETS
 To overcome PTI, pathogens deliver specialized effectors (apoplastic or
cytosolic) that cause disease via effector-triggered susceptibility (ETS).
 Effectors interfere with defense through various spatial/temporal
mechanisms depending on the pathogen and effector.
 Some effectors open natural openings like stomata for apoplastic entry.
Others move cell-to-cell through intercellular connections.
 The Phytophthora brassicae effector RxLR3 interacts with PD-localized
callose synthases to inhibit callose and promote symplastic trafficking in
leaves.
 PWL2 and BAS1 effectors from the rice blast fungus accumulate at the
biotrophic interface then move symplastically from cell to cell, ahead of
infection hyphae in some cases.
 Effector movement depends on size and cell type - some uniformly
express while others translocate selectively.