Resistance to Soybean Cyst Nematode: Rhg1

The genes underlying rhg1 lie at a sometimes dominant sometimes co-dominant locus, necessary for resistance to all Hg types of the soybean (Glycine max (L.) Merr.) cyst nematode (Heterodera glycines). Genomic research identified; nucleotide changes within a candidate gene encoding a receptor like kinase (RLK) that were capable of altering root development and thereby part of the resistance to Hg types 0 (race 3); changes in a laccase that are capable of altering cyst development; and genes underlying changes in membrane biology. This set of three genes are subject to co-selection with a modifier locus on another linkage block. Root development is slowed in the resistant seedling and results in end of season yield loss when SCN is not present. However, in the presence of SCN resistant seedling roots grow just as vigorously as the now slower growing parasitized susceptible roots and therefore show little loss to SCN parasitism. In some genotypes but not others the RLK can act alone to confer resistance. Functional paralogs of the three gene cluster have been found on other linkage groups including A1, B1, G, and O and these can be functional in different sources of resistance like G. soja, PI 437654 and PI438489B. At rhg1 the allele differences change the structure, interacting partners and activity of the LRR protein and the laccase. The changes between the alleles result in about 30 other proteins (judged by 2 Dgels), 112 metabolites (by FTICRMS) and 8 metabolites (by GCMS) to increase in abundance in roots during SCN infection in the resistant NILs. Understanding the basis of root stunting by resistance alleles will be used to improve methods for developing new nematode resistant soybean cultivars that do not suffer from the yield suppression and low seed germination rates of existing cultivars.

Identification of graminicide-resistant johnsongrass (Sorghum halepense)

Resistance to fluazifop-P and quizalofop-P, (aryloxyphenoxypropionates) and sethoxydim (cyclohexanedione) was identified in 2 populations of johnsongrass in both field and greenhouse studies. The cropping history (1983–1991) of the sites indicated 1 or more annual applications of a graminicide (primarily fluazifop-P) since the early 1980s. Under field conditions, control of resistant seedling and rhizome johnsongrass (R91F) with fluazifop-P, quizalofop-P, fenoxaprop-ethyl, and sethoxydim was less than 35%. Clethodim provided up to 80% control of R91F. Under greenhouse conditions, ratios (R/S) of the I50values (amount of herbicide required to inhibit plant growth by 50%) of resistant (2 sites: R91F and R91S) to susceptible (S91H) seedling (20–30-cm height) plants were > 388 (fluazifop-P), > 15 (quizalofop-P), and from 2.3 (R91S) to 3.4 (R91F) (both sethoxydim). For rhizome (30–45 cm height) plants, the R/S ratios were > 388 (fluazifop-P), > 16 (quizalofop-P), and 2.8 (R91S) to 8.5 (R91F) (both sethoxydim). Labeled rates (in kg ai ha−1) of fluazifop-P (0.10 and 0.21), quizalofop-P (0.039 and 0.08), and sethoxydim (0.21 and 0.21) were applied on seedling and rhizome plants, respectively, and resulted in little or no control of resistant johnsongrass. Greenhouse studies indicated registered rates of clethodim (0.10 and 0.14 kg ai ha−1for seedling and rhizome plants, respectively) effectively controlled the resistant populations, but tolerance was measured for both seedling and rhizome plants at sublethal doses (down to 0.007 and 0.009 kg ai ha−1, respectively), with I50ratios ranging from 1.5 (R91S) to 2.1 (R91F) for seedling plants and 4.5 (R91S) to 4.8 (R91F) for rhizome plants. Control of resistant seedling and rhizome johnsongrass under field conditions was adequate with glyphosate at 0.84, glufosinate at 0.84, and sulfosate at 0.84 kg ai ha−1, indicating no cross-resistance.

RESISTANCE TO POWDERY MILDEW IN PERENNIAL PHLOX

Forty-nine cultivars of perennial phlox, Phlox paniculata L., grown in a field plot at Ottawa were compared for resistance to powdery mildew in 1961, 1962, and 1963. None of the cultivars was immune. A seedling, designated by the number 60–75, showed field resistance to mildew that was significantly better than the other cultivars for 3 years but subsequently became susceptible. A second cultivar, Pyramid White, initially showed field resistance to powdery mildew but it became susceptible to the disease more quickly than 60–75. Results obtained under the conditions of our experiments suggested that first-year plants were more resistant to powdery mildew than plants of the same cultivars that were at least 3 years old. In breeding for resistance, only a few seeds from crosses germinated but one apparently resistant seedling was obtained. However, this seedling subsequently became susceptible.

The Mechanism of Host Penetration by Thanatephorus Cucumeris

Evidence is presented in support of the hypothesis that chemical stimuli control the development of infection structures on the host surface by T. cucumeris. On the stem of a young radish seedling there are discrete, susceptible a�reas which become fewer and eventually disappear as the seedling ages. Rubbing the stems of radish seedlings with or without an organic solvent increases the number of infection cushions formed by a crucifor-attacking isolate, and returns an older resistant seedling to the susceptible condition. No infection cushions form on strips of cuticle and epidermis removed from the host.