dynamics with research and extension programs
C.R. Wellings{ XE "Wellings, C.R." }A,B and K.R. KandelBA
NSW Department Primary Industries, seconded to
B
The University of Sydney, Plant Breeding Institute, PMB 11, Camden, NSW 2570
INTRODUCTION
Wheat stripe rust (caused by Puccinia striiformis f. sp. tritici, Pst)
was first recorded in Australia in 1979 and became endemic to
the eastern Australian wheat zone causing serious losses in the
mid eighties (1). Concerted pathology and breeding R&D
combined with industry adoption of resistant varieties resulted
in minimal losses for nearly 20 years. The first report of stripe
rust in Western Australia in 2002 was the result of a foreign
pathotype incursion (2). This aggressive pathotype widened its
distribution in following years to encompass the entire
Australian wheat production zone, and caused serious losses
including increased annual fungicide expenditure ranging from
$AUD40–90million (1).
The stripe epidemic in eastern Australia in 2008 was the most
intensive in the 30 year history of the disease in Australia. The
dynamics of host resistance and pathogen variability gave rise to
a situation that required a close connection between extension
and research staff in order to maximise the available resources
of host resistance and fungicide availability. This paper presents
details of the epidemic development and the interplay of variety
resistance and pathogen population dynamics during the 2008
season.
MATERIALS AND METHODS
Rust samples collected and forwarded to PBI by co‐operators
(advisors, farmers, researchers) were assessed for pathotype
determination using described methods (3). Results were
immediately reported to co‐operators by email. The relationship
between pathotype and the resistance genes present in
commercial wheats provided a basis for predicting expected
disease response.
RESULTS AND DISCUSSION
Samples received from various regions of Australia are illustrated
in Figure 1. The epidemic began early from presumed green
bridge survival sites, developed slowly in winter, and became
explosive in spring; the epidemic was largely confined to NSW
and Queensland.
Figure 1. Frequency of Pst samples accessioned at PBI Rust Laboratory in
2008 from six regions in Australia.
The major pathotypes detected in the 2008 epidemic are
described in Table 1.
Table 1. Features and frequency of the four Pst pathotypes detected in
Australia in 2008. (R=resistant; S=susceptible)
Resistance Gene (Yr) Response Pathotype First Report 2008 n=830 17 J 27 ‘WA’ 2002 20% R R R ‘WA Yr17’ 2006 12% S R R ‘Jackie’ 2007 55% R S R ‘Jackie Yr27’ 2008 <1% R S S
The ‘Jackie’ pathotype dominated the population, despite only
its second season of detection in Australia. This pathotype is
adapted to triticales and became established early 2008 on long
season triticales (carrying the YrJ resistance) and wheats sown
for dual purpose grazing and grain. Since this pathotype
dominated the Pst population, wheats carrying the Yr17
resistance remained resistant, especially in the early phase of
the epidemic. However the ‘WA Yr17’ pathotype re‐emerged in
spring and varieties carrying this gene were sprayed to ensure
yield protection.
The first detection of the ‘Jackie Yr27’ pathotype in 2008 raises
concerns for wheats carrying Yr27, ie Ruby, Merinda, Waagan.
However the combined resistance of Yr17 and Yr27 in Livingston
wheat will be expected to provide protection to all pathotypes
detected in 2008.
Continuing studies to determine the resistances deployed in
commercial agriculture, monitoring pathotype dynamics during
seasonal development and clear communications with the
extension community provides an important basis for disease
control recommendations.
ACKNOWLEDGEMENTS
This work forms part of the Australian Cereal Rust Control
Program funded by the Australian Grains Research and
Development Corporation.
REFERENCES
1. Wellings CR (2007) Puccinia striiformis in Australia: A review of the incursion, evolution and adaptation of stripe rust in the period 1979–2006. Australian Journal of Agricultural Research 58: 567– 575.
2. Wellings CR, Wright G, Keiper F, Loughman R (2003) First detection of wheat stripe rust in Western Australia: evidence for a foreign incursion. Australasian Plant Pathology 32:321–322.
3. Wellings CR, McIntosh RA (1990) Puccinia striiformis f.sp. tritici in Australasia: pathogenic changes during the first ten years. Plant
Pathology 39:316–325. 0 20 40 60 80 100 120 May June July Augu st Sept embe r Octo ber Nove mbe r Dece mbe r S a mp le N u mb e r Queensland n NSW s NSW Victoria South Australia Western Australia
Session
6A—Cereal
pathology
Impact of sowing date on crown rot losses
S. Simpfendorfer{ XE "Simpfendorfer, S." }NSW Department of Primary Industries, 4 Marsden Park Rd, Tamworth, 2340, NSW
INTRODUCTION
Crown rot caused by the fungus Fusarium pseudograminearum
(Fp) is a major constraint to winter cereal production in the
northern cropping region especially under no‐till farming
systems (3). Yield loss from crown rot interacts heavily with
moisture stress during grain‐fill. One way to manipulate this
interaction is through sowing time. Only two studies have ever
examined this interaction under natural field infections which
both found that earlier sowing increased the incidence of crown
rot (1,2). An issue with these previous studies is that they are
unable to differentiate seasonal interactions from the direct
crown rot effects. An inoculated versus uninoculated
experimental design, as suggested in (2), was adopted in this
study to allow the direct effects of crown rot to be determined
on yield and quality across three sowing dates.
MATERIALS AND METHODS
Three bread wheat varieties (EGA Gregory, Strzelecki and EGA
Wylie) were used with the first two being longer season and
rated as being more susceptible to crown rot and EGA Wylie a
main season variety which has the best resistance rating. Plots of
each variety were either uninoculated or inoculated with
sterilised durum grain colonised by Fp at a rate of 2g/m of row.
Plots of each treatment were then sown on three different dates
at Tamworth in 2008 being: 1st sowing = 21st May, 2nd sowing =
10th June and 3rd sowing = 27th June. There were four
replicates of each treatment which were blocked for sowing time
with treatments randomised within each block. Hand samples
were removed from each plot at physiological maturity to obtain
pathology measures while yield and quality were obtained from
samples collected using a small plot harvester.
RESULTS
Good rainfall occurred at Tamworth late in the season during
grain‐fill which prevented the formation of whiteheads in all
treatments. There was no significant variety x inoculum or
variety x sowing time x inoculum effect on yield given this good
finish to the season. Sowing time had a significant impact on
final grain yield in all three varieties with the average percentage
yield reduction between the 1st and 2nd sowing for the three
varieties being ‐9% and between the 1st and 3rd sowing ‐22.6%.
Crown rot had less of an impact on yield at each sowing date
causing ‐4.1% yield loss at 1st sowing, ‐3.4% 2nd sowing and ‐
6.7% at 3rd sowing date.
Percentage screenings were also significantly affected by sowing
time (1st to 2nd sowing date +1.0%; 1st to 3rd sowing date
+3.5%). Crown rot also had a direct effect of increasing
screenings at each sowing date with a trend towards increased
negative impacts with delayed sowing (1st +0.7%, 2nd +1.5% and
3rd +1.7%).
There was no difference between the three varieties in the levels
of infection initiated by Fp at any sowing date i.e. longer season
varieties did not have greater numbers of plants infected
irrespective of sowing time. In plots where no additional Fp
inoculum was added (background infections) there was no
difference in the percentage of plants infected at harvest
between the three sowing times. When Fp inoculum was added,
all sowing times resulted in around 80% of plants or greater
being infected at harvest with the 2nd sowing time being
significantly higher at 94% than the other two sowing times.
However, with both inoculum levels it was obvious that early
sowing did not result in increased numbers of infected plants at
harvest.
Although early or delayed sowing time did not impact on the
percentage of plants ultimately infected by Fp, it did appear to
influence disease expression as measured by the extent of basal
browning (i.e. crown rot severity). Delaying sowing time
significantly increased disease severity across the three sowing
dates at both inoculum levels.
DISCUSSION
Sowing time and hence length of exposure to infection over the
season did not result in different levels of plants being infected
by Fp at harvest. The 2008 season was very conducive to
infection with good soil moisture for much of the year. Certainly
longer season varieties and earlier sowing did not increase
susceptibility to infection.
Earlier sowing increased yield and reduced screenings
irrespective of crown rot infection. The actual % yield loss to
crown rot did not vary greatly between sowing times with each
of the varieties. There was an indication that crown rot resulted
in increased screenings with later sowings. The 2008 season was
not overly conducive to yield and quality loss from crown rot but
differences were still evident. It would be interesting to repeat
this experiment in a season with a tougher finish. In theory,
bringing grain‐fill forward even 1–2 weeks may have a
considerable impact on disease expression by limiting moisture
and evaporative stress.
The major effect on yield and quality comes from the sowing
time itself. Later sowing decreases yield potential and grain size
and increases screenings. Adding crown rot into the picture on
top of this further exacerbates these losses thus increasing the
probability of downgrading. The % yield and quality losses
attributable to crown rot were pretty consistent across the three
sowing dates. If anything they got slightly worse with the later
sowings. Hence, sowing earlier in the window, if soil moisture
allows, maximises the genetic yield potential, grain size and
limits screenings in a variety. This provides buffering from any
detrimental effect that crown rot infection may then have.
ACKNOWLEDGEMENTS
Partial funding for this research was provided by the Grains
Research and Development Corporation.
REFERENCES
1. Purss GS (1971) Effect of sowing time on the incidence of crown rot (Gibberella zeae) in wheat. Australian Journal of Experimental
Agriculture and Animal Husbandry 11, 85–89.
2. Klein TA, Burgess LW, Ellison FW (1989) The incidence of crown rot in wheat, barley and triticale when sown on two dates. Australian
Journal of Experimental Agriculture 29, 559–563.
3. Burgess LW, Backhouse D, Summerell BA, Swan LJ (2001) Crown rot of wheat. In: Fusarium. (Ed BA Summerell, JF Leslie, D Backhouse, WL Bryden, LW Burgess) APS Press. pp 271–294.