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ing pathways, although exceptions do exist (Mur et al. 2006 ; Leon-Reyes et al. 2010 ;
Verhage et al. 2010 ). The suppression of JA/ET-regulated defenses confers suscep-
tibility to many tissue-damaging and phloem-feeding herbivores (Howe and Jander
2008; Zarate 2007; Gao et al. 2007 ; Pieterse and Dicke 2007 ) and can influence at-
traction of natural enemies (Zhang et al. 2009 ). However, in some plant—herbivore
interactions, SA-regulated defenses and/or novel defense-signaling pathways con-
tribute to the plant immune response (Thaler et al. 2010 ; Bhattarai et al. 2007 , 2010 ).
Therefore, the nature of defenses elicited by endosymbiont-like pathogens in their
host plants have the potential to profoundly impact the plant's interaction with the
insect and/or ability to resist attacks by other pathogens or pests. If an herbivore can
circumvent induced plant defenses or plant recognition by vectoring its endosym-
biont associate into its host plant during feeding, it may have a selective advantage
relative to insects feeding on uninfected plants. Alternatively, effectors from the
endosymbiont may circumvent the plant recognition system, compromising plant
immune responses and related insect and bacterial resistance in both the JA/ET- and
SA-regulated defense pathways. Thus, the endosymbiont's modification of plant
defenses could result in a more susceptible host plant for both symbiotic partners.
Understanding Pathogenesis: Role of Systems Biology
The Fusarium spp. causes disease to crops (Table 8.1 ) and the disease effect is huge
in terms of economy due to problems in health to animals as well as humans by con-
suming the contaminated grain (McMullen et al. 1997 ) with mycotoxins (Garvey
et al. 2008 ). Thus, it becomes necessary to understand pathogenesis (pathogenic
genes) and thereby prevent the invasion by these destructive pathogens. The plant
pathology discipline describe the pathogenesis genes as those which causes losses
or in other words are those which when disrupted causes the reduction of disease
symptoms (Idnurm and Howlett 2001 ). The identification of these genes can be
done with either the gene silencing or gene knockout studies (Liu et al. 2010 ). In
F. graminearum 49 pathogenic genes have been verified by utilizing the biologi-
cal methods and then stored in PHI-base database (http://www.phi-base.org/query.
php). However, when we consider the genome size of F. graminearum , it is real-
ized that compilation of the pathogenesis related genes is a huge uphill task as well
as time consuming. To solve this problem, the computational biological methods
could provide an alternative for solving this problem, especially after the release
of genome sequences in Broad Institute (http://www.broadinstitute.org) (Liu et al.
2010 ). Hence, for the prediction of pathogenesis genes comparative genomics will
be handy and will help in comparison between fungi, which are either pathogenic or
non-pathogenic (Zhao et al. 2008b , c ). But, recently it has been found that it is dif-
ficult to identify pathogenesis genes in F. graminearum because there are no unique
features in specific genes among pathogenic and non-pathogenic fungi (Liu et al.
2010 ). On the basis of literature on pathogenicity in model pathogens (Gohre and
Robatzek 2008 ), it can be believed that F. graminearum pathogenesis is also involv-
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