© Benaki Phytopathological Institute
Al-Doude
et al.
74
and is closely associated with redox homeo-
stasis, hypersensitive response, or system-
ic acquired resistance (Alvarez, 2000; Dong,
2004).
Semi quantitative RT-PCR analysis dem-
onstrated that attack of barley by
P. teres
in-
duced
PR2
accumulation in infected plants
as compared with the un-infected controls
and it was inversely regulated 24h post inoc-
ulation i.e, it was repressed in the susceptible
cultivar WI2291 while being induced in the
tolerant genotype Banteng (
Fig. 3
). More-
over, RT-PCR expression analysis revealed
that the
PR2
expression increased in the re-
sistant and susceptible genotypes over the
inoculation time points, with the highest ex-
pression (6.4 and 1.99–fold for Banteng and
WI2291, respectively) observed at 6 dpi.
PR2
Figure 1.
a) Frequency of disease reactions incited on barley (a) resistant cv. Banteng and (b) susceptible cv. WI2291, 10
days after
Pyrenophora teres
infection. b) Disease symptoms on the resistant (BAN) and susceptible (WI) barley genotypes,
which were measured using the scale described by Abu Qamar
et al
. (2008).
Figure 2.
Quantification of total salycilic acid in barley leaves 1, 2, 3 and 4 days post inoculation with
Pyrenophora teres
in
(a) the resistant cv. Banteng and (b) the suscepitible cv. WI2291. Error bars represent the stantard error of the means (
n =
3
).
