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members of the family Brassicaceae whereas responsiveness to Ax21 seems
confi ned to rice (Kunze et al. 2004 ; Zipfel 2008 ; Segonzac and Zipfel 2011 ).
Flagellin induces resistance in Arabidopsis , tobacco, tomato, and rice. The PAMP
rhamnolipids were able to stimulate defense genes in tobacco, wheat, grapevine,
and Arabidopsis thaliana (Vatsa et al. 2010 ).
The specifi city of particular PAMP may be due to its specifi city towards its PRR
in plants. The PRR EFR for the PAMP EF-Tu has been detected in plants belonging
to the family Brassicaceae. The transfer of EFR from Brassicaceae to Solanaceae
species confers a broad-spectrum resistance to phytopathogenic bacteria in
Solanaceous plants (Lacombe et al. 2010 ). The results suggest that EFR is impor-
tant in triggering plant immune responses and its action is not specifi c to particular
plants. Similarly the PRR Xa21 gene is detected in rice plants and the PAMP Ax21
activates plant immune responses in rice. Transgenic Citrus sinensis plants express-
ing the rice Xa21 gene were developed and these transgenic plants also conferred
resistance against the citrus bacterial pathogen Xanthomonas axonopodis pv. citri
(Mendes et al. 2010 ). The results suggest that the PRR from one plant species can
be transferred to another plant species to extend the usefulness of PRRs in manage-
ment of wide-spectrum of pathogens in a wide range of plants.
2.30
Role of PAMPs and Effectors in Activation of Plant
Innate Immune Responses
Pathogen effectors are proteins and small molecules that alter host-cell structure
and function. These alterations either facilitate infection or trigger defense
responses or both (Hogenhout et al. 2009 ; Boureau et al. 2011 ). Effectors are
double-edged swords that enhance virulence of pathogens in susceptible plants and
trigger resistance in plants carrying cognate resistance (R) proteins (Zong et al.
2008 ). Effector-triggered immunity (ETI) and PAMP-triggered immunity (PTI) are
two branches of the plant immune system. PTI uses transmembrane PRRs that
respond to PAMPs, whereas ETI acts largely inside the cell, using polymorphic
nucleotide binding-leucine-rich repeat (NB-LRR) protein products encoded by
most R (resistance) genes (Jones and Dangl 2006 ). These NB-LRR proteins have
been targeted by breeders for decades to elicit resistance to crop pathogens in the
fi eld (Tör et al. 2009 ). The ETI was formerly known as gene-for-gene resistance
(Boller and He 2009 ).
Interactions between plants and pathogens can be classifi ed as compatible,
incompatible, and nonhost interactions. Incompatible interactions are cultivar-
specifi c and determined by ETI. In contrast, compatible interactions are thought to
lack ETI. Nonhost interactions refer to those between a plant species and non-
adapted pathogens. Some effectors from nonadapted pathogens also trigger ETI and
induce HR, typically seen in the incompatible interactions (Zhang et al. 2010b ).
Effector-triggered immunity results in amplifi cation of PTI and it constitutes the
second layer of defense (Day and He 2010 ).
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