ABA Regulation of Plant Response to Biotic Stresses - Abscisic Acid: Metabolism, Transport and Signaling - page 401

1 h after exposure to pathogenic and non-pathogenic bacteria (Melotto et al.
2006 , 2008 ; Schulze-Lefert and Robatzek 2006 ; Zeng et al. 2010 ; Faulkner and
Robatzek 2012 ). Furthermore, perception of several pathogen- or microbe-associ-
ated molecular patterns (PAMPs or MAMPs), such as the flagellin derivative flg22
and lipopolysaccharides, can rapidly induce stomatal closure and then activate
stomatal innate immunity (Melotto et al. 2006 ; Zeng et al. 2010 ). Interestingly,
besides of its prominent role in regulating stomatal closure upon drought stresses
(Schroeder et al. 2001 ), several studies have also demonstrated the involvement of
ABA in stomatal innate immunity. For example, the Arabidopsis mutants defec-
tive in ABA synthesis ( aba3 - 1 ) or ABA signaling ( ost1 - 2 ) are unable to perceive
two PAMPs, flg22 and lipopolysaccharide, and fail to induce stomatal closure.
Thus, it is evident that ABA can positively prevent pathogen infection by function-
ing in PAMP-induced stomatal closure (Melotto et al. 2006 ). The ABA-controlled
PAMP-induced stomatal closure required several key steps, including ABA syn-
thesis, NO production, and the OST1 kinase (Melotto et al. 2006 ). Similarly, SA
can also induce stomatal closure, and the SA-deficient mutants eds5 - 1 , eds16 -
1 / sid2, and NahG transgenic plants, or SA signaling mutants, such as npr1 , show
impaired ability in closing the stomata in response to the Pst DC3000 or PAMPs,
indicating the important role of SA in stomatal innate immunity (Melotto et al.
2006 ; Zeng et al. 2010 ). Further studies demonstrated that the SA signaling regu-
lator NPR1 acts downstream of SA, but upstream of ABA in stomatal immunity
(Zeng and He 2010 ). Recently, it was reported that the rhizobacteria Bacillus
subtilis FB17-mediated stomatal closure involved both SA and ABA signaling
(Kumar et al. 2012 ). However, the mechanism of possible cross talk between SA
and ABA during stomatal innate immunity is still unclear.
In turn, pathogens have evolved a variety of virulence factors to counteract
stomatal innate immunity and finally colonize the host tissues through reopening
the stomata. Pst DC3000 can reopen stomata by producing the effector molecule
coronatine (Melotto et al. 2006 ; Zeng and He 2010 ). Recent study demonstrated
that Pst DC3000 can also produce another effector HopM1 to reduce both bacte-
rial PAMP flg22 and the fungal PAMP chitin-induced stomatal closure (Lozano-
Durán et al. 2013 ). Similarly, Xanthomonas campestris pv. campestrisis ( Xcc ) can
also overcome stomatal innate immunity through a DSF cell-to-cell signal-regu-
lated virulence factor which has the ability to revert bacteria, lipopolysaccharide,
or ABA-induced stomatal closure (Gudesblat et al. 2009 ). The bacterial citrus
pathogen, X. axonopodis pv. citri , can produce a plant natriuretic peptide (PNP)
to antagonize ABA-dependent stomatal closure and finally create a favorable host
environment for its own survival (Gottig et al. 2008 ). Some fungal pathogens also
use virulence factors, such as fusicoccin and oxalate, to counteract stomatal clo-
sure (Turner et al. 1969 ; Guimaraes et al. 2004 ). Hence, based on these reports,
we can deduced that ABA functions in stomatal innate immunity by controlling
stomatal closure upon pathogen infection while some successful pathogens have
evolved virulence factors to counteract stomatal innate immunity. The ABA-
mediated stomatal innate immunity constitutes an important part of the plant pre-
invasive penetration resistance (Ton et al. 2009 ).