Biomedical Engineering Reference
In-Depth Information
plants (Walton 1994). The impact of rapid advances in fungal genomic
technologies enables the identification of numerous new candidate
genes potentially involved in disease (Trail et al. 2003). The sequence of
the genome of F. oxysporum was released in 2007 by the Broad Institute
( http://www.broad.mit.edu) and this information allowed the creation
of deletion constructs, knocked out, and breakage of secretion pathway
of enzyme in order to analyze their function. Besides, techniques of
recombinant DNA have been employed to try to provide evidence
concerning the role of CWDE in plant pathogenesis. Due to the functional
redundancy of isoenzymes in microbes, disruption of one or more CWDE
genes in a pathogen leads to virulence. Nevertheless, gene disruption
experiments have provided convincing evidence that CWDEs are involved
in pathogenicity.
Roncero et al. (2003) observed the degradation of cell wall components
(xylan, cellulose, pectin) after Fusarium oxysporum infection in, postulating
that the secretion of CWDE played a role during penetration and disease
establishment. Different enzymatic pathways and their corresponding gene
channels have been detected in Fusarium oxysporum, these gene channels
regulates enzymatic machinery that can degrade polysaccharides on the
cell wall (MarĂ­n et al. 1998, Roncero et al. 2000, 2003). Hellweg (2003)
analyzed extra-cellular alkaline proteases of Fusarium by biochemical and
genetic methods. Fusarium spp. perforates the host cell wall and invades the
endosperm in the fi eld, producing a large amount of CWDE, host toxins,
or both (Hammond-Kosack and Jones 2000). Pathogens mainly obtain their
nutrients from cytoplasmic proteins, starch and fats, which can be utilized
only after degradation by enzymes secreted by the pathogen.
GENES OF FUSARIUM OXYSPORUM CODING
CELL WALL DEGRADING ENZYMES RESPONSIBLE
FOR WILTING IN PLANTS
Fusarium oxysporum Schlecht causes vascular wilt diseases in a wide variety
of crops (Beckman 1987). Based on host specifi city, more than 120 different
formae speciales of F. oxysporum has been recognized (Armstrong and
Armstrong, 1981). The soil-borne pathogen survives as chlamydospores,
and germinates upon stimulus by the crop host to infect plants through
their root systems. Infection most commonly takes place through wounds,
but direct penetration is known to occur in some Fusarium wilt diseases
(Pennypacker and Nelson 1972). To enter plant cells directly, F. oxysporum
genes have to regulate the enzymatic pathways in order to produce a
wide variety of extracellular cell wall degrading enzymes (CWDEs),
including endo- and exopolygalacturonases (PGs), xylanases, cellulases,
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