**Session V -- Effective Pest (Pathogen, Insect, Weeds) Management --
Talk: Pacheco**

**Partial Resistance to Crown Rust -- Identification, Utilization and
Genetics**

Marcelo T. Pacheco^1^, Marty L. Carson^2^, Eric W. Jackson^3^, James
Chong^4^

^1^ Department of Plantas de Lavoura, Federal University of Rio Grande
do Sul, Brazil; E-mail: marpac@ufrgs.br

^2^ USDA-ARS, Cereal Disease Lab, 1551 Lindig St, Saint Paul, MN, US,
55108; E-mail: Marty.Carson@ars.usda.gov

^3^ USDA-ARS, 1691 S 2700 W, Aberdeen, ID, US, 83210; E-mail:
Eric.Jackson@ars.usda.gov

^4^ Cereal Research Centre, Agriculture & Agri-Food Canada, 195 Dafoe
Road, Winnipeg, MB, Canada; Email: jchong@agr.gc.ca

Control of crown rust (*Puccinia coronata* f.sp. *avenae*) with
race-specific seedling genes (*Pc* genes) has proven to be effective for
only 3-5 years once a cultivar becomes widely grown. Partial resistance
to crown rust, a special case of incomplete resistance, is an
alternative to major genes and has been proposed as a strategy to obtain
longer lasting control of the disease. The ideal type of partial
resistance would also be race non-specific and behave as adult plant
resistance. This presentation summarizes the efforts of four different
research groups which are directly involved in identifying, better
understanding, and transferring new sources of partial crown rust
resistance into elite germoplasm. Two of these groups are located in the
US, one in Canada, and the other in Southern Brazil. The Brazilian group
has been able to recognize new partial resistance sources among highly
adapted germplasm. Selection is performed in field plots under natural
infection where partially resistant genotypes are mainly identified
during routine screening of segregating populations in the breeding
program, searching for visual indication of mechanism that leads to
sporulation reduction, such as flecks, strong chlorosis around the
pustules and pustule death. The group has been successful using this
methodology and preliminary work indicates that resistance may result
from the additive effect of small-effect genes, which confer adult plant
resistance. Both US groups belong to USDA-ARS. At the Cereal Disease Lab
(CDL) in Minnesota, work has been carried out to distinguish between
true partial resistance and race-specific resistances, which correspond
to virulences at a low frequency in the field. To achieve this, oat
accessions that have exhibited low rust severity were tested in trials
where plots were inoculated with a crown rust inoculum specifically
selected for virulence on seedlings of that accession. One of the main
challenges is the successful introgression of partial resistance from
these sources into elite material, but preliminary results suggest it is
possible to combine high levels of partial resistance with acceptable
agronomic characteristics. The research group located at the USDA-ARS in
Aberdeen, Idaho, developed a new methodology to increase the accuracy in
mapping crown rust resistance loci. Phenotyping crown rust resistance
can be affected by several variables, such as non-uniform disease
development in the field, atypical symptom development in the
greenhouse, presence of multiple races of the pathogen in the field, and
rater experience. To overcome these limitations, the new system consist
of the artificial production of single race polycyclic field epidemics
coupled with detailed assessment of uredia length on infected flag
leaves and fungal DNA estimates using quantitative PCR (q-PCR). Results
from QTL mapping of crown rust resistance showed improved QTL detection
in single race studies compared to multi-location field tests. A study
on the genetics of the partial/slow-rusting resistance in the oat line
GS1 from Purdue University was carried out at the Cereal Research
Centre, Agriculture & Agri-Food Canada. GS1 was found to have
race-specific resistance in greenhouse tests, expressing both seedling
and adult plant resistance. Results of the genetics study using a GS1/AC
Morgan BC~?~F~?~ population indicate that partial resistance in GS1 is
controlled by two loci, not being possible to distinguish between the
two models: 1) one recessive gene (aa) with dominant gene (BB)
suppression; 2) two complementary loci, one being dominant (AA) and the
other being recessive (bb). A study is ongoing to determine which model
is correct.