Page 9 - Volume 7, Issue 1, January 2014

© Benaki Phytopathological Institute
Evolution in P. halstedii 7
able to demonstrate how new virulent rac-
es may have emerged, it was not possible to
ascertain from these data at what frequency
such events occur, or if crosses between cer-
tain races are more likely than others.
New endemic races could also arise
through clonal evolution, a ubiquitous pro-
cess in the evolution of many pathogens.
Evolution of virulence by accumulation of
mutations has been previously described
for rusts such Puccinia striiformis where 20
different pathotypes were found to have
arisen from a single introduction followed
by a stepwise mutation process (Steele et
al., 2002). Mutation is the ultimate source of
genetic variation, directly leading to chang-
es in the DNA sequence of an individual
gene and thus creating new alleles in pop-
ulations. The mutation accumulation sug-
gests that the evolutionary effect of adverse
events declines following the age at which
an organism is initially capable of reproduc-
tion (McDonald and Linde, 2002). Further-
more, recent evidence for race emergence
in P. halstedii was recently demonstrated
by infecting an experimental plot with rac-
es 100 and 710. After 5 years six other races
were observed (300, 304, 314, 700, 704, 714)
that had not been present at the start of the
study (Tourvieille de Labrouhe et al., 2010).
Although there is no sufficient data to con-
clude that this mechanism has led to race
emergence in situ, it appears to be a plausi-
ble explanation given that these genotypes
have not arisen by recombination. Further-
more, in the absence of selection pressure,
Sakr et al. (2011) reported that P. halstedii did
not evolve its virulence. This rapid evolution
of virulence in P. halstedii was revealed in
France exerted by the intensive Pl genes re-
sistance selection pressure; fifteen different
races of this pathogen have now been char-
acterized, nine of which emerged in the last
ten years (Delmotte et al., 2008). Concern-
ing the influence of Pl genes selection pres-
sure on aggressiveness of P. halstedii, Sakr et
al. (2011) suggested that the method of Pl
gene management affects aggressiveness
of pathogen populations because it deter-
mines the number of susceptible plants har-
bored by the parasite.
Concerning the influence of quantita-
tive resistance of aggressiveness of P. hals-
tedii, few studies were carried out. Indeed,
Sakr (2012a) analyzed the quantitative com-
ponent of pathogenicity for P. halstedii iso-
lates of the race 710; it was found that the
index of aggressiveness varied significant-
ly among the isolates. The differences be-
tween the more aggressive and less aggres-
sive isolates of sunflower downy mildew is
likely to be matter of extreme differences
evident in quantitative resistance in culti-
vated sunflower cultivars. It seems that the
quantitative resistance selection pressure in
sunflower cultures could vary in aggressive-
ness in P. halstedii isolates of the race 710 as
observed for Venturia inaequalis (Parisi et al.,
2004). The selection pressure by both: qual-
itative and quantitative resistance in sun-
flower plants may modify the two compo-
nents of pathogenicity in P. halstedii .
Relationships among the morpholog-
ical, genetic and pathogenic traits in P.
halstedii
Different attempts were made to cor-
relate pathogenic variability including vir-
ulence and aggressiveness traits with mor-
phological and genetic levels. However,
from an epidemiological perspective, it is
important to know whether variability at
the pathogenic level is just neutral variabil-
ity or whether it is related to other pheno-
typic traits. In plant pathogens, some stud-
ies have revealed the relationship between
the two components of pathogenicity: vir-
ulence and aggressiveness. Sullivan et al.
(2005) found a negative relationship be-
tween virulence and aggressiveness for Phy-
tophthora parasitica var. nicotianae on to-
bacco and a positive case for Phakospora
pachyrhizi on soybean (Bonde et al., 2006).
For sunflower downy mildew, the relation-
ship between virulence and aggressive-
ness was found to be positive or negative
and two hypotheses were made to explain
them (Sakr, 2011c). First, it seems that vir-
ulence and aggressiveness are independ-
ent, and the coincidence makes this relation