© Benaki Phytopathological Institute
Evolution in
P. halstedii
9
2011a,b,c, 2012a,b,c, 2013), important dif-
ference in pathogenicity affects sunflower
plant’s response by showing an importance
for
Pl
gene to differentiate among patho-
gen isolates for virulence (Tourvieille de La-
brouhe
et al.,
2010; Sakr, 2011b; Franchel
et
al.,
2013) and by masking the impact of ge-
netic factors underlying QTL for aggressive-
ness (Vear
et al.,
2008; Vincourt
et al.,
2012).
Results obtained in recent studies (Sakr
2009, 2011a,b,c, 2012a,b,c, 2013) could be
used in a strategy that helps to improve du-
rability of sunflower resistance to downy
mildew (Vincourt
et al
., 2012; Franchel
et
al
., 2013). Results presented by Sakr (2009,
2011a,b,c, 2012a,b,c, 2013) showed that vir-
ulent groups had different levels of aggres-
siveness. Understanding principal caus-
es which explain the intervention between
virulence and durability of sunflower plants
is crucial. Qualitative
Pl
resistance genes in
sunflower plants were the main keys for the
emergence of new and endemic
P. halstedii
races in response to recombination facilitat-
ed by pathogen introductions as noted re-
cently by Ahmed
et al.
(2012). Indeed, the
potential of
P. halstedii
to evolve new races
has also been enhanced by the introduction
of several genetically differentiated geno-
types: repeated introductions of
P. halstedii
isolates, combined with the selective pres-
sure exerted by host resistance genes, may
have greatly accelerated the breakdown of
qualitative resistance (Ahmed
et al.,
2012).
Exploring aggressiveness variation of sun-
flower downy mildew populations may pro-
vide significant knowledge about host re-
sistance mechanisms and the potential
breakdown of resistance. Because quantita-
tive resistance is likely to play a prominent
role in future breeding programs, it might
be important to assess resistance against
diverse
P. halstedii
populations, including
challenging breeding material with
P. hal-
stedii
isolates collected from wild
Helianthus
species, because they are more aggressive
than those from other host species and may
include diverse mechanisms with the poten-
tial to break the qualitative sunflower resis-
tance. Moreover, Sakr (2011b) reported that
dynamic of evolution in
P
.
halstedii
isolates
showing new virulence and carrying differ-
ent levels of aggressiveness is correlated
with qualitative and quantitative selection
pressure.
Recently, Sakr (2012b) proposed a mix-
ture model of sunflower inbred lines carry-
ing the two types of resistance (qualitative
and quantitative). This sunflower model may
enhance durable resistance against
P. halste-
dii
. This strategy supposes that pathogenic-
ity of
P. halstedii
would slowly and difficult-
ly develop on sunflower genotypes carrying
qualitative and quantitative resistance. Con-
sequently, it would limit fungal capacity to
reproduce and disperse among the plants of
a mixture.
Although
P. halstedii
has an evolutionary
capacity to produce new virulent races un-
der the selection pressure of
Pl
genes (Gu-
lya, 2007), it seems that the ability of path-
ogen to develop its pathogenicity may be
limited by the presence of the two types
of resistances in our mixture model. The
sunflower inbred lines carrying effective
Pl
genes could prevent the dispersion of more
aggressive pathotypes in
P. halstedii
. In addi-
tion, the sunflower inbred lines showing dif-
ferent levels of quantitative resistance could
limit the reproduction and dispersion of vir-
ulent pathotypes in sunflower downy mil-
dew. Super races present the most difficult
hindrance for the cultivation of sunflower
on a large surface. Indeed, the agricultural
system containing the two types of resist-
ance in a given environment may provide
a satisfactory control for the development
of the parasite. Also, this model may reduce
costs of sunflower production by improving
the best conditions that limit the reproduc-
tion of the pathogen.
Conclusions
Even though a big step has been made to-
wards understanding the complex inter-
action of
P. halstedii
with sunflower, as well
as the mechanisms of pathogenicity evo-
lution, a number of questions still remaine
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