(RLKs) or receptor-like proteins (RLPs) [3, 5]. Lysine motifs (LysM) or lectin motifs
are common extracellular domains in RLKs and RLPs; the extracellular motif is the
most characterized domain in plants [6, 7]. PRRs can perceive also self-molecular
signatures termed as damage-associated molecular patterns (DAMPs), which are
plant cell wall fragments produced as a result of mechanical damage or enzymatic
degradation by microbial activities [4, 5]. PRR-mediated microbe perception
induces a comprehensive defense responses in plants called MAMP- or PAMPtriggered immunity (MTI/PTI) [5]. MTI/PTI leads to early plant defense signaling
which is initiated with variations in the plasma transmembrane potential (Vm),
promoting intracellular Ca
2+ influx; these events eventually lead to the massive
transcriptional reprogramming that initiates defense responses such as production
of antimicrobial secondary metabolite, stomatal closure, and thickening of the cell
wall [8–10]. MTI/PTI prevents non-adapted microbes from infecting and is therefore
an important barrier against disease. The adopted pathogens overcome the MTI/PTI
responses by batteries of virulence factors known as effectors [9]. Host plants
evolved to win back the arm race with the adopted microbes by host-specific
intracellular receptor (R) proteins that sense effectors and trigger a defense against
adopted microbes called effector-triggered immunity (ETI) [9, 11] (Scheme 1).
2.1
Early Response to Bacteria
The PRR flagellin-sensitive 2 (FLS2) is one of the most well-studied plant PRRs.
FLS2 binds to bacterial flagellin (flg22) and promotes the formation of LRR
receptor-like kinase (RLK) and brassinosteroid-insensitive 1 (BRI1), which acts as
a co-receptor for flg22 and is essential for the full activation of MTI signaling [12]. It
has been shown that the phosphorylation of the plant LRR kinase FLS2 is rapid,
occurring within 15 s of stimulation with flg22 [13]. Other PRRs involved in the
early perception of bacteria include the elongation factor-Tu (EF-Tu) receptor (EFR),
which perceives bacterial EF-Tu and its peptide epitope elf18 [5]. The application of
flg22 and elf18 induced a transient depolarization in Arabidopsis mesophyll cells
and root hairs after a delay of approximately 1–3 min [14].
Plants perceive peptidoglycans (PGNs) which are a major constituent of bacterial
cell walls. Plants employ several receptors to perceive PGNs. For instance, in
Arabidopsis, PGN is perceived by two LysM-RLPs (AtLYM1 and AtLYM3) [15]
and in rice by two LysM-RLPs (OsLYP4 and OsLYP6) [16]. The PGN-induced
responses in Arabidopsis also require the LysM-RLK chitin elicitor receptor kinase 1
(CERK1), which failed to bind PGN itself [15].
2.2
Early Response to Fungi
Chitin is a major component of fungal cell walls and has been recognized as a
general elicitor of plant defense responses for many years [17]. Different plants have
evolved distinct mechanism of chitin perceptions. For instance, fungal chitin-related
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S. A. Zebelo
are common extracellular domains in RLKs and RLPs; the extracellular motif is the
most characterized domain in plants [6, 7]. PRRs can perceive also self-molecular
signatures termed as damage-associated molecular patterns (DAMPs), which are
plant cell wall fragments produced as a result of mechanical damage or enzymatic
degradation by microbial activities [4, 5]. PRR-mediated microbe perception
induces a comprehensive defense responses in plants called MAMP- or PAMPtriggered immunity (MTI/PTI) [5]. MTI/PTI leads to early plant defense signaling
which is initiated with variations in the plasma transmembrane potential (Vm),
promoting intracellular Ca
2+ influx; these events eventually lead to the massive
transcriptional reprogramming that initiates defense responses such as production
of antimicrobial secondary metabolite, stomatal closure, and thickening of the cell
wall [8–10]. MTI/PTI prevents non-adapted microbes from infecting and is therefore
an important barrier against disease. The adopted pathogens overcome the MTI/PTI
responses by batteries of virulence factors known as effectors [9]. Host plants
evolved to win back the arm race with the adopted microbes by host-specific
intracellular receptor (R) proteins that sense effectors and trigger a defense against
adopted microbes called effector-triggered immunity (ETI) [9, 11] (Scheme 1).
2.1
Early Response to Bacteria
The PRR flagellin-sensitive 2 (FLS2) is one of the most well-studied plant PRRs.
FLS2 binds to bacterial flagellin (flg22) and promotes the formation of LRR
receptor-like kinase (RLK) and brassinosteroid-insensitive 1 (BRI1), which acts as
a co-receptor for flg22 and is essential for the full activation of MTI signaling [12]. It
has been shown that the phosphorylation of the plant LRR kinase FLS2 is rapid,
occurring within 15 s of stimulation with flg22 [13]. Other PRRs involved in the
early perception of bacteria include the elongation factor-Tu (EF-Tu) receptor (EFR),
which perceives bacterial EF-Tu and its peptide epitope elf18 [5]. The application of
flg22 and elf18 induced a transient depolarization in Arabidopsis mesophyll cells
and root hairs after a delay of approximately 1–3 min [14].
Plants perceive peptidoglycans (PGNs) which are a major constituent of bacterial
cell walls. Plants employ several receptors to perceive PGNs. For instance, in
Arabidopsis, PGN is perceived by two LysM-RLPs (AtLYM1 and AtLYM3) [15]
and in rice by two LysM-RLPs (OsLYP4 and OsLYP6) [16]. The PGN-induced
responses in Arabidopsis also require the LysM-RLK chitin elicitor receptor kinase 1
(CERK1), which failed to bind PGN itself [15].
2.2
Early Response to Fungi
Chitin is a major component of fungal cell walls and has been recognized as a
general elicitor of plant defense responses for many years [17]. Different plants have
evolved distinct mechanism of chitin perceptions. For instance, fungal chitin-related
580
S. A. Zebelo