II. 40. Response to selection for virulence against the ml-o based mildew resistance in barley, not fitting the gene-for-gene hypothesis.

Erik Schwarzbach, Lehrstuhl für Pflanzenbau und Pflanzenzuchtung, Technische Universität Munchen, 805 Freising-Weihenstephan, FRG. "R"

The recessive ml-o allele, known as a frequent mutation in barley, described first by Freisleben and Lein (1942) and found later also among barley from Ethiopia (Nover and Schwarzbach, 1971), was believed to provide a nonspecific resistance against mildew (Favret 1971). Indeed, no corresponding virulence was found so far among mildew isolates from Europe, Near East, North America and Japan and in field observations at 78 locations in Europe, Near East, the Americas, New Zealand and Japan (Jørgensen 1977). However, Wolfe and Schwarzbach (1978) suggested that this might be due to absence of selection pressure for ml-o virulence, since ml-o barleys are not commercially grown. To test this hypothesis a large scale selection experiment over 37 cycles was started with a pure mildew isolate from a 'Carina' field and with the barley line HLN 70-8, derived from the ml-o mutant SZ5139b (Schwarzbach 1967). To allow for rare virulence mutations, about 10⁷ mildew spores were applied in a settling tower to several hundreds of primary leaves of the ml-o host in each cycle. During the first 15 cycles the resulting sporadic pustules were multiplied on a susceptible host to provide enough inoculum for the next cycle. From the 16th cycle on, the conidia, harvested from the ml-o host were used directly as inoculum for the next cycle. The response was monitored by the percentage of conidia, forming secondary elongating hyphae (ESH), using iodine stained replicas (Schwarzbach and Kendlbacher, 1977). The response is demonstrated on Figure 1. In spite of irregularities, due to environmental effects, the trend is evident.

Figure 1. Response to selection for increased virulence in the barley mildew culture HL-2 through repeated reinfection cycles on a host with ml-o based mildew resistance.

Since a part of it might be due to improved conditions of growth and infection, the virulence of the population after 37 cycles of selection was compared with that of the original culture. The virulence was monitored by the ESH percentage and by the mildew multiplication rate, estimated from inoculation density and resulting sporulation per area. The experiment was repeated 4 times and the results summarized in Table 1. The data reveal an increase in both the number of successful infections per 100 applied spores and in spore production per colony. The total virulence (sporulation per area) is about 30 times higher than in the original culture.

Table 1. ml-o virulence of a mildew population after 37 cycles of selection, compared with that of the original culture.

For one mutational event and its selection a sigmoid response curve would be expected, according to the formula given by Wolfe and Schwarzbach (1978). To find, if indeed more mutations for ml-o virulence are present, pure mildew isolates were taken from the selected population and tested for ml-o virulence in 4 times repeated experiments. The results are summarized in Table 2.

Table 2. Performance of 6 isolates from a mildew population selected in 37 cycles for ml-o virulence, compared with the original culture.

The data show the presence of at least 4 mildew genotypes. differing in at least 3 genes for ml-o virulence and differing in their effectiveness. This is in contrast with the gene-for-gene hypothesis, permitting just one gene of the parasite to interact with a resistance gene of the host. A similar array of isolates, differing widely in their effectiveness against the Mla gene of 'Tyra' barley, was reported by Schwarzbach et al. (1978). The reason why in genetic experiments usually just 1 gene of a parasite is found to interact with a host resistance gene, may be that the less effective virulence mutations are finally lost from a population by competition since they most likely originate in different individuals that reproduce vegetatively during the course of selection.

References:

Favret, E.A. 1971. Different categories of mutations for disease reaction in the host organism. Mutation Breeding for Disease Resistance. IAEA Wien 1971:107-116.

Freisleben, R. and A. Lein. 1942. Über die Auffindung einer mehltauresistenten Mutante nach Roentgenbestrahlung einer anfälligen reinen Linie von Sommergerste. Naturwiss. 30:608.

Jørgensen, H.J. 1977. Spectrum of resistance conferred by ml-o powdery mildew resistance genes in barley. Euphytica 26:55-62.

Nover, Ilse and E. Schwarzbach. 1971. Inheritance studies with a mildew resistant barley mutant. Barley Genetics Newsl. 1:35-37.

Schwarzbach, E. 1967. Recessive total resistance of barley to mildew (Erysiphe graminis D.C. f. sp. hordei Marchal) as a mutation induced by Ethylmethansulfonate. (Czech). Genetika a slechteni 3:159-162.

Schwarzbach. E., J.A. Barret and M.S. Wolfe. 1978. Evolutionary response of pathogens to disease control. 3rd Internat. Congr. of Plant Pathol., Munchen, 16-23 August 1978.

Schwarzbach, E. and R. Kendlbacher. 1977. Die Untersuchung früher Entwicklungsstadien des Mehltaues auf Blattoberflachen mit dem Jodabdruckverfahren. Z. Pflanzenz. 78:83-87.

Wolfe, M.S. and E. Schwarzbach. 1978. The recent history of the evolution of barley powdery mildew in Europe. In: D.M. Spencer (Ed.), The Powdery Mildews. Acad. Press, 565 pp.

BGN 9 toc
BGN Main Index