Biomedical Engineering Reference
In-Depth Information
biosynthesis. Pathogen-induced ethylene is presumed to play a major role
in wilt disease development. The mutants defective in
VdPKAC1
showed
reduced conidia but higher numbers of microsclerotia compared with wild
type strain. Another gene, the sucrose nonfermenting 1 gene in
V. dahliae
(
VdSNF1
) was characterized recently using ATMT and clearly demonstrated
that it plays a crucial role in pathogenicity of this fungus (Tzima et al. 2011).
The growth of the
vdsnf1
mutants was signifi cantly reduced in different
carbon source media. The virulence was severely affected in
VdSNF1
deleted
mutants and showed defective early stage colonization of tomato roots.
Several genes required for pathogenicity have been identifi ed in
V.
dahliae
with the employment of ATMT (Maruthachalam et al. 2011a). From
this study, two pathogenicity genes of
V. dahliae
, endoglucanase 1 (
VdEg1
)
and hydroxy methylglutaryl-CoA synthase gene (
VdHMGS
) were identifi ed
as pathogenicity-associated genes based on virulence phenotype. Several
other putative candidate genes for pathogenicity have also been identifi ed
through this study such as major facilitator superfamily transporter (MFS
transporter), RasGTPase-activating protein (
RasGAP1
), mannosyltransferase
3 (
GPI
) etc., and detailed characterization of these genes is currently
underway.
Identifi cation and Characterization of Genes in
M. oryzae
Several groups have conducted large-scale insertional mutagenesis using
ATMT and reported patterns of T-DNA insertion into the genome of
M.
oryzae
(Choi et al. 2007, Jeon et al. 2007, Li et al. 2007, Meng et al. 2007).
From these and other works combined with phenotype screening for
T-DNA mutants, a number of genes including pathogenicity genes were
identifi ed and further characterized in this fungus as listed in
Table 3.
This list includes only the genes whose functions and contributions to
pathogenicity are investigated in detail, following large-scale insertional
mutagenesis and phenotype screenings.
Previous studies on pathogenicity genes had focused on the genetic
components of cellular signaling pathways based on reverse genetics
approach. These efforts showed how well-conserved signaling pathways
regulate infection-related morphogenesis of the fungus in response to
environmental cues and host-dependent constraints. However, reverse
genetics approaches are inadequate for revealing novel aspects of molecular
mechanisms underlying fungal pathogenicity, since these approaches rely
on a prior knowledge of the functions of characterized orthologues. ATMT
does not require such knowledge and thus is not biased in identifying
pathogenicity genes. Though the numbers are small, genes and their
functions listed in Table 3 show that pathogenicity is not a simple trait
that can be understood by looking at a few signaling pathways but a
