Investigations Into the Genetic Basis of Resistance to Brown Stem Rot in Soybean
Patzoldt, Megan Elise
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https://hdl.handle.net/2142/85015
Description
Title
Investigations Into the Genetic Basis of Resistance to Brown Stem Rot in Soybean
Author(s)
Patzoldt, Megan Elise
Issue Date
2004
Doctoral Committee Chair(s)
Diers, Brian W.
Department of Study
Crop Sciences
Discipline
Crop Sciences
Degree Granting Institution
University of Illinois at Urbana-Champaign
Degree Name
Ph.D.
Degree Level
Dissertation
Keyword(s)
Agriculture, Plant Pathology
Language
eng
Abstract
These studies examine the inheritance of brown stem rot (BSR) resistance in soybean [Glycine max (L.) Merr.], caused by a soil-borne fungal pathogen Phialophora gregata f. sp. sojae. Three known BSR resistance genes or quantitative trait loci (QTL) have all been mapped together on linkage group (LG) J. Although genetic resistance to BSR is not well understood, it has been successfully deployed as a method of control. Understanding the genetics of resistance to BSR and identifying new sources of resistance are key components of successful BSR control strategies. Objectives of these studies were to: screen 85 accessions from the germplasm collection with multiple highly virulent biotypes of P. gregata f. sp. sojae to identify accessions with the strongest resistance; localize BSR resistance QTL from 'Bell', a resistant cultivar with genetic background from PI 88788; develop a BSR/soybean cyst nematode (SCN) co-inoculation method and examine if SCN increases BSR symptoms in two near isogenic line populations; determine if five resistant accessions from central China contain BSR resistance on LG J; test the proposed four gene model for inheritance of resistance to BSR in two half-sib populations of F2:3 lines; re-make the PI 88788 by 'Williams' cross and study the inheritance of BSR resistance in the progeny. From the first study, ten accessions were identified with levels of BSR resistance greater than or equal to known resistance sources. The second study revealed a BSR resistance QTL from Bell was localized to an area on LG J where the three BSR resistance genes have been mapped. The third study demonstrated the presence of SCN caused a numeric increase in the expression of BSR disease symptoms. All 5 accessions in study four were found to contain BSR resistance QTL on LG J as previously described. Data from the two half-sib populations was better supported by a multiple QTL model than by the proposed four gene model for BSR resistance in the fifth study. The final study revealed BSR resistance was controlled by a major LG J resistance QTL from P188788 and by multiple minor affect QTL inherited from Williams.
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