Biology Reference
In-Depth Information
Chapter 2
PAMP Signaling in Plant Innate Immunity
Abstract Plant innate immunity is a potential basal defense system existing in
plant kingdom. This system provides powerful weapons to the host plants to fi ght
against viral, bacterial, fungal, and oomycete pathogens and serves as a surveil-
lance system against invasion of pathogens. It is not active in normal healthy plants
and it requires specifi c signals to get activated. Pathogen-associated molecular
patterns (PAMPs) act as alarm/danger signals to trigger the plant innate immune
responses. When pathogens land on the plant's surface, plants read the molecular
fi ngerprints/signatures of pathogens (PAMPs) by binding the PAMPs with cognate
pattern-recognition receptors (PRRs) residing in plant cell plasma membrane and
trigger several defense signaling systems. Pathogens contain a wide array of
PAMPs of diverse chemical structures and every pathogen contains or secretes
multiple PAMPs. Each PAMP may regulate induction of different defense genes.
The time of induction, intensity of induction, and duration of induction of the
defense signals may vary depending on PAMPs. Amount of PAMP available in the
plant-pathogen interaction site may determine the intensity of induced gene expres-
sion. Each PAMP may regulate distinctly different signaling pathway(s). Sometimes
different PAMPs may induce the same signaling system, but the intensity of the
defense signaling gene expression may differ. The same PAMP may behave differ-
ently in different plant system. A single PAMP may not be able to activate all the
defense signaling-related genes and several PAMPs may be required to activate the
complex signaling systems. PAMPs may act synergistically or antagonistically in
inducing defense signaling. Some PAMPs have additive effect, while others show
antagonistic effect between them. The PAMPs are perceived as danger signals by
PRRs and the PAMP-PRR complex activates the plant innate immunity. PAMPs
trigger phosphorylation of PRRs. Fine control of membrane-resident PRR activity
is essentially achieved by a combination of proper endoplasmic reticulum (ER)
folding, degradation and traffi cking of PRRs. Strict elimination of the misfolded
PRR occurs in the absence of the identifi ed ER folding machineries, which would
avoid precocious immune activation. Pre-recognition membrane traffi c of PRRs
from the ER to their functional sites, together with post-recognition internalization
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