Avirulence
genes in plant pathogens have been defined by their requirement for disease
resistance in hosts containing corresponding R genes. Plant viruses evolve very
rapidly owing to very short replication cycles, large numbers of genomes within
each cell across many cells per host, and many hosts. For RNA viruses, the
absence of a proofreading function in viral replicases may result in mutation
rates as high as 104 per replication cycle per base. Viral genetic variation
can result from several major genetic processes including mutation,
recombination, and the acquisition of additional genomic sequence. As a
consequence, resistance breaking viral genotypes are known for most host
resistance, especially for genes showing HR. Avirulence determinants are
typically identified by creating chimeric clones derived from viral genotypes
with contrasting virulence and then testing for infectivity. Once an avirulence
domain is identified, site-directed mutagenesis allows identification of
specific point mutations responsible for virulence.
Virtually any part of the viral genome can
define an avirulence determinant. With respect to R genes that confer HR,
avirulence factors include viral RNA polymerase subunits, movement protein, and
CP. Several potyviral avirulence genes have been identified for dominant R
genes that do not show HR. The CI and P3 proteins of Turnip mosaic virus serve
as avirulence determinants for the Brassica napus R genes, TuRBO1 and
TuRBO4/5 (96–98), while SMV HC-Pro and P3 are involved in overcoming Rsv1
in soybean. In contrast to the case for dominant genes where many different
viral components have been identified as avirulence determinants, a pronounced
trend is apparent viral factors that serve as the determinant for pathogenicity
in resistance systems controlled by recessively inherited R genes. Of nine R
gene studies to date, seven identify potyviral VPg as the pathogenicity
determinant for recessive resistance, although the systems in question show
diverse resistance phenotypes: Capsicum pvr1/pvr12 resistance to PVY is
cellular, tobacco va resistance impairs the cell-to-cell movement, and Nicandra
physaloides and Solanum commersonii affect long-distance movement.
The eighth study, also focused on a potyviral system, PsbMV/pea, identified the
P3-6K1 cistron as the pathogenicity determinant. Only one study to date has
focused outside the Potyviridae. In this case, the 3_ untranslated region of
the carmovirus Melon necrotic spotvirus (MNSV) genomic RNA defined the
location of the viral determinant in the by interaction of MNSV with melon. In
the eight cases where the viral elicitor is protein, host recognition of these
viral proteins that serve as pathogenicity determinants is altered by amino
acid substitutions that do not appear to significantly compromise the function of
the protein in pathogenesis. For other microbial pathogens, there often appears
to be a fitness penalty association with mutations from avirulence to virulence.
Although this type of fitness/avirulence tradeoff has not been noted generally
for plant viruses, there are specific examples where this occurs. Isolates of
ToMV capable of overcoming Tm22 gene were found to multiply poorly on
resistant plants. If the Tm22 resistant protein targets a domain of the
viral MP such that this protein is mutated to overcome resistance, these
mutations could result in diminished fitness.