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Published in Crop Sci 30:575-578 (1990)
© 1990 Crop Science Society of America
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Gene Frequency Changes in Soybean Bulk Populations Exposed to Phytophthora Rot

T. C. Kilen* and B. L. Keeling

USDA-ARS, Soybean Production Res. Unit, P.O. Box 196, Stoneville, MS 38776

* Corresponding author.

Phytophthora rot (caused by Phytophthora megasperma Drechs. f. sp. glycinea Kuan & Erwin) frequently causes severe injury to soybean [Glycine max (L.) Merr.]. Screening populations for resistance genes in cultivar improvement programs is labor intensive, and alternative systems would be desirable. The objective of this study was to determine the shift in frequencies of two genes controlling resistance to phytophthora rot when segregating soybean populations were advanced on fields naturally infested with the pathogen. ‘Tracy’ (having resistance genes Rpsl-b and Rps3) was crossed with ‘Forrest’ and a highly susceptible breeding line, D55-1492. Forrest has no known genes for resistance to phytophthora rot, but shows minimal injury from the disease in field plantings where D55-1492 shows stand loss or is severely stunted. Populations were advanced on clay soil known to be predominantly infested with Race 1 of the pathogen. To identify individual genes, 200 randomly selected plants from each population were harvested individually and their progeny inoculated with Races 2 and 7. A shift to a higher frequency of the Rpsl-b allele, but not Rps3, was observed after 5 yr of advance in the Tracy x DSS-1492 cross. No shift to a higher frequency occurred in the Tracy x Forrest cross, suggesting that the field resistance of Forrest was competitive with genetic resistance. The results indicate that the frequency of phytophthora-resistance genes can be effectively increased under natural disease pressure if the population segregates for highly susceptible plants (or if disease pressure is much greater than in the environments sampled).


Joint contribution of the USDA-ARS and the Delta Branch, Mississippi Agric. Forestry Exp. Stn., Stoneville.

Received for publication June 12, 1989.





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