Page 10 - Volume 7, Issue 1, January 2014

Sakr

8

positive and negative. Second, there is an ef-

fect of additional virulence genes in

P. hals-

tedii

races for variation of aggressiveness as

observed for other pathogens (Brown and

Tellier, 2011). Knowledge of virulence cost,

trade-off between virulence and aggres-

siveness, would help to understand the dy-

namics of sunflower downy mildew popula-

tions that use their pathogenicity to better

improve adaptation to their environment.

Indeed, Van der Plank (1968) defined the

cost of virulence as reduction in pathogen

fitness induced by a mutation from an aviru-

lence state to virulence, and the changes in

pathogen aggressiveness resulting direct-

ly from the loss of avirulence gene function.

Indeed, Sakr (2012c) found that the 100 and

3xx avirulent races had a virulence cost mea-

sured by differences in aggressiveness (from

58.3 to 78.2%, depicts aggressiveness from

the virulent to a virulent state) compared

to 7xx virulent races carrying unnecessary

virulence gene. However, accumulation of

virulence genes results in reduced aggres-

siveness as observed for

Puccinia graminis

f.

sp.

avenae

(Leonard 1969),

Bipolaris maydis

(Leonard 1977),

Puccinia graminis

f.sp.

triti-

ci

(Grant and Archer 1983) and for

Erysiphe

graminis

f. sp.

hordei

(Grant and Archer 1983).

Usually in a gene for gene interaction, viru-

lence cost in new races comes from loss (and

not accumulation) or mutation of avr genes

that might contribute to virulence (Stahl

and Bishop 2000). The trade-off between

virulence and aggressiveness probably has

considerable consequences for

P. halstedii

evolution, because races that accumulate a

large number of virulence genes might nev-

er be the most aggressive on sunflower gen-

otypes. Moreover, it seems that negative re-

lationship between the two components of

pathogenicity may play an important role in

generating local adaptation in the pathosys-

tem of

P. halstedii

and sunflower by imped-

ing the emergence and evolution of races

that are both highly aggressive and capable

of multiplying on all sunflower genotypes.

Regarding the correlation between

pathogenicity traits and genetic variability,

Sakr (2011a, 2013) found no correlation be-

tween molecular genotypes and pathoge-

nicity traits. The low degree of association

between traits of virulence and aggressive-

ness and the molecular variation is expedit-

ed considering the high degree of variation

in pathogenicity of

P. halstedii

. However, the

lack of matching between pathogenicity

traits and groups based on molecular mark-

ers was not surprising. Indeed, Montarry

et

al

. (2006) did not find a clear correlation be-

tween phenotypes and genotypes based

on molecular markers for

Phytophthora in-

festans

.

Pathogenicity is known to evolve

through mutation without highly altering

molecular fingerprints (Goodwin, 1997). Be-

cause most molecular markers used for fin-

gerprinting are selectively neutral, they can

be used to assess evolutionary forces other

than selection (such as gene flow or genetic

drift). Concerning the correlation between

pathogenicity traits and morphological

characteristics in sunflower downy mil-

dew races, Sakr (2013) found no correlation

between morphological genotypes and

pathogenicity traits. Sakr (2013) found that

the proportion of zoosporangia of different

forms and their sizes and the morphology of

sporangiophores do not appear to be use-

able to differentiate the virulent character-

istics for

P. halstedii

isolates. The results also

showed that zoosporangia and sporangio-

phores morphology did not distinguish the

aggressiveness groups. Regarding the cor-

relation between morphological traits and

genetic variability, Sakr (2013) found no cor-

relation between molecular genotypes and

morphological traits.

Durable resistance in sunflower against

Plasmopara halstedii

Regarding the intervention between

pathogenic variation in

P. halstedii

and dura-

bility of resistance in sunflower plants, new

data (Sakr, 2009, 2011a,b,c, 2012a,b,c, 2013)

showed that large variation in pathogenic-

ity has been detected within and between

P. halstedii

races. Such variation could arise

due to the agroecological environment,

host diversity, cultural practices, and sexu-

al recombination. According to Sakr (2009,