Variability in Fusarium species Causing Wilt Disease in Crops: A Transcriptomic Approach to Characterize Dialogue Between Host and Pathogen - Crop Improvement: New Approaches and Modern Techniques - page 276

by the living cells. The plants have effective defense mechanisms to limit the spread
of parasitic fungi and they have to encounter the primary line of defense provided
by cell wall of host plants, which inhibit their penetration to the tissues. The second-
ary line of defense includes the production of wide range of secondary metabolites
or compounds which act as fungicides. These compounds are induced, that is they
are produced only after the infection has occurred (e.g. Phytoalexins). The fungal
parasites are host specific and some of them even require the alteration of hosts,
which may or may not be phylogenetically related for stage wise development on
either host. The fungal pathogens have been seen to cause more damage to agri-
culture (monocultures) than in plant communities rich in species due to high host
specificity. To get hold of the plant nutrients the fungal parasites are having at least
three strategies. (1) Production of enzymes for cell wall and cuticle breakdown. (2)
Production of toxins to either reduce or inhibit the cellular activity. (3) Production
of host-specific substances (e.g. phytohormones) and thus disturbing the hormonal
equilibrium and thus causing disruption of growth and differentiation of the cells
and tissues (e.g. Gibberella fujikuroi ) produces gibberellins which affect the growth
of rice. The literature about pathogenicity of fungi is very extensive and majority of
these emphasize on economic considerations, classification, life cycle, symptoms
and diagnostic, host range and factors of host resistance. The processes of plants
molecular mechanisms after infection have been elucidated in recent past and these
can be partially generalized due to variation in possible interaction reactions. The
host resistance is not only based on general and unspecific defense mechanisms
but also on specific mechanisms during which genetically determined substances
are produced which are directed against specific fungal pathogen. Genetic analyses
have shown that the host resistance is caused by genes inherited independently of
each other, such as the existence of dominant alleles of the respective genes, and
resistance genes. It has been shown by microarray analysis that resistance to virus in
melon is associated with defense responsive gene expression/induction (Gonzalez-
Ibeas et al. 2012a ) which led to development of a cost-effective kit for microar-
rays (Gonzalez-Ibeas et al. 2012b ). Further, the silenced lines of melon developed
by RNA Interference showed resistance against the viruses (Rodriguez-Hernandez
et al. 2012 ). Plants protect themselves against the diversity of herbivores and mi-
crobial pathogens by expressing an array of constitutive and induced defenses ren-
dering the plant an inaccessible or unsuitable food source. The perception of attack
and deployment of the induced defenses is primarily mediated by three well-studied
defense-signaling pathways that are regulated by jasmonic acid (JA), salicylic acid
(SA) and ethylene (ET) (Glazebrook 2005 ; Howe and Jander 2008 ; Walling 2009 ).
Herbivores and pathogens introduce a distinct set of elicitors and effectors that are
perceived by host plants and these signals allow the plant to tailor its defense re-
sponse to individual challengers (Glazebrook 2005; Howe and Jander 2008; Wall-
ing 2009; McSteen 2008 ; Zhao et al. 2008a; Stout et al. 2006 ; Bari and Jones 2009 ).
The SA-regulated defense pathway is activated by biotrophic pathogens (pathogens
that invade living plant tissue) and many phloem-feeding insects (Glazebrook 2005;
Walling 2009; Kempema et al. 2007 ; Puthoff et al. 2010 ; Kusnierczyk et al. 2008 ;
Zarate 2007 ). Often SA-induced signaling antagonizes JA- and ET-regulated signal-