TY - JOUR
T1 - Evaluation of spring cereal grains and wild Triticum germplasm for resistance to Rhizoctonia solani AG-8
AU - Smith, J. D.
AU - Kidwell, K. K.
AU - Evans, M. A.
AU - Cook, R. J.
AU - Smiley, R. W.
PY - 2003/3
Y1 - 2003/3
N2 - Rhizoctonia root rot, caused by Rhizoctonia solani Kühn AG-8 (Anastomosis Group 8), is a yield-limiting disease of direct-seeded cereals in the Pacific Northwest (PNW) region of the USA, and to date, no resistant Triticum germplasm has been identified. The objective of this research was to identify potential sources of genetic resistance among selected members of the primary, secondary, and tertiary gene pools of wheat (Triticum aestivum L.) for use in cultivar improvement. Members of the primary gene pool {spring wheat germplasm, synthetic hexaploids, triticale (x Triticosecale spp.), Triticum turgidum var. durum (Desf.) Bowden [= T. turgidum subsp. durum (Desf.) Hush.]}, secondary gene pool [Aegilops cylindrica Host, Dasypyrum villosum (L.) P. Candargy], and tertiary gene pool (Hordeum vulgare L.) of wheat were screened for disease response to two isolates (C1 and D2) of R. solani AG-8 in controlled environment assays. Variation for magnitude of susceptibility to both isolates was detected, but no sources of resistance were identified among primary or tertiary gene pool members. Isolate D2 generally produced more severe disease than isolate C1, with the exception of the most susceptible accessions for which both isolates caused equally severe disease. All accessions of D. villosum exhibited some level of seedling resistance to isolate C1, and 73% also displayed a resistance response to isolate D2. All D. villosum/durum amphiploids, as well as Chinese Spring/D. villosum addition lines, were susceptible to both isolates. Differences in disease response between the two isolates suggest that varying levels of virulence, or aggressiveness, exist among R. solani AG-8 isolates.
AB - Rhizoctonia root rot, caused by Rhizoctonia solani Kühn AG-8 (Anastomosis Group 8), is a yield-limiting disease of direct-seeded cereals in the Pacific Northwest (PNW) region of the USA, and to date, no resistant Triticum germplasm has been identified. The objective of this research was to identify potential sources of genetic resistance among selected members of the primary, secondary, and tertiary gene pools of wheat (Triticum aestivum L.) for use in cultivar improvement. Members of the primary gene pool {spring wheat germplasm, synthetic hexaploids, triticale (x Triticosecale spp.), Triticum turgidum var. durum (Desf.) Bowden [= T. turgidum subsp. durum (Desf.) Hush.]}, secondary gene pool [Aegilops cylindrica Host, Dasypyrum villosum (L.) P. Candargy], and tertiary gene pool (Hordeum vulgare L.) of wheat were screened for disease response to two isolates (C1 and D2) of R. solani AG-8 in controlled environment assays. Variation for magnitude of susceptibility to both isolates was detected, but no sources of resistance were identified among primary or tertiary gene pool members. Isolate D2 generally produced more severe disease than isolate C1, with the exception of the most susceptible accessions for which both isolates caused equally severe disease. All accessions of D. villosum exhibited some level of seedling resistance to isolate C1, and 73% also displayed a resistance response to isolate D2. All D. villosum/durum amphiploids, as well as Chinese Spring/D. villosum addition lines, were susceptible to both isolates. Differences in disease response between the two isolates suggest that varying levels of virulence, or aggressiveness, exist among R. solani AG-8 isolates.
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M3 - Article
AN - SCOPUS:0037339559
SN - 0011-183X
VL - 43
SP - 701
EP - 709
JO - Crop Science
JF - Crop Science
IS - 2
ER -