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2. Plant materials: Plant
materials used were Triticum aestivum (L.) Thell. cv. Norin 4
(N4), cv. Red Egyptian (RE), and ditelocentrics of cv. Chinese Spring
(CS). Infection types of N4, RE, and CS with Tk-1, Ak-1, Gw-180, and
Gw-121 are shown in Table1.
Pm10 is a gene for resistance to f.sp. agropyri
identified with another F1 culture, Gw-34 (Tosa et al.
1987), but does not operate against Gw-180 nor Gw-121.
3. Determination of infection types: Seeds of test plants were
germinated on a wet filter paper in a petri dish for a few days.
After root tips were removed for cytological examination, seeds with
roots were sown in soil in 2 x 35 em test tubes. Five to six days
after sowing, primary leaves of the test plants were inoculated with
conidia from 8-day-old colonies of Gw-180 or Gw-121 using writing
brushes. The seedlings were grown in a controlled-environment room
under fluorescent lighting (2000-4000 lux) before and after
inoculation. The temperature in the room was 23 plus or minus1C
during the light cycle (13 hr) and 20 plus or minus1C during the dark
cycle (11 hr). Eight days after inoculation, infection was rated
using 13 progressive grades from 0 to 4: 0, no mycelial growth or
sporulation; 0+, mycelial growth without sporulation; 1-,
conidiophore formation without visible powder-like conidia; 1,1+,
scant sporulation; 2-,2,2+, reduced sporulation; 3-,3,3+, slightly
reduced sporulation; 4-,4, heavy sporulation.
Results and Discussion
For mapping of Pm11 (controlling the resistance to Gw-180)
ditelo 6BS of CS (resistant to Gw-180) was pollinated with N4
(susceptible to Gw-180), and the resulting F1 plants were
backcrossed with N4. The B1F1 plants were
examined cytologically and then inoculated with Gw-180
(Table
2). All of the
seedlings that did not carry the telosome were susceptible (infection
types 2+ to 4), and most of the seedlings carrying it were resistant
(infection type 0). These results suggested that genetically Pm11
on chromosome 6B short (Tosa et al. 1988) was closely linked to
the centromere. The distance between the centromere and Pm11
was calculated to be 0.98cM or 0.98 map unit. However, the gene may
not be located in the chromosomal region near the centromere because
crossing over is highly suppressed in the sat-chromosomes.
For mapping of Pm15 (controlling the resistance to Gw-121)
ditelo 7DS of CS (resistant to Gw-121) was pollinated with RE
(susceptible to Gw-121), and the resulting F1 plants were
backcrossed with RE. The B1F1 plants were
examined cytologically and then inoculated with Gw-121. Although the
number of B1F1 seedlings tested were small, it
was apparent that the telosome and the resistance to Gw-121 were
segregated independently (Table
2). The recombination
value was 50%. These results suggested that Pm15 on chromosome
7D short (Tosa and Sakai 1990) was very distant from the
centromere.
Acknowledgments
The authors thank Dr. U. Hiura, emeritus professor of Okayama
University, Okayama, and Dr. K. Tsunewaki, emeritus professor of
Kyoto University, Kyoto, for providing the common wheat
cultivars.
References
Tosa Y, Tsujimoto H and Ogura H (1987) A gene involved in the
resistance of wheat to wheatgrass powdery mildew fungus. Genome
29:850-852.
Tosa Y, Tokunaga H and Ogura H (1988) Identification of a gene for
resistance to wheatgrass powdery mildew fungus in the common wheat
cultivar Chinese Spring. Genome 30:612-614.
Tosa Y (1989) Genetic analysis of the avirulence of wheatgrass
powdery mildew fungus on common wheat. Genome 32:913-917.
Tosa Y and Sakai K (1990) The genetics of resistance of hexaploid
wheat to the wheatgrass powdery mildew fungus. Genome 33:225-
230.
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