In a recent publication Torp and Jørgensen (1986) reported on 25 mutants more or less powdery mildew susceptible selected from the resistant barley line 'Sultan-5', which has the semi-dominant powdery mildew resistance gene M1-a12 conferring an infection type 0 (1-2 cn when heterozygous) with avirulent powdery mildew. Ten of the mutants were analyzed genetically by Torp and Jørgensen (1986). The remaining 15 mutants have subsequently been analyzed (Jørgensen 1987). The main results will be summarized in the following, together with an interpretation.

Firstly, the 25 mutants had infection types between 0-1 n, i.e., close to that of the mother line, and 3-4 cn, i.e., close to compatibility, but no mutant was fully compatible with M1-a12 avirulent pathogen isolates. Further, with M1-a12 virulent pathogen isolates all mutants were susceptible, i.e., indistinguishable from the mother line. The virulent isolates comprised avirulence corresponding to the resistance genes M1-2, through M1-a14, except gene M1-a8, i.e., all 11 alleles" described in locus M1-a. This shows that all 25 mutants had retained the race-specificity of gene M1-a12; only the phenotypic expression of gene M1-a12 was changed.

Secondly, twenty-two of the mutants had each one mutant gene allelic to gene M1-a12. This was proven by the segregation in F2 populations from crossing the mutants with the mother line 'Sultan-5'. The results imply that the M1-a12 "locus" constitutes an allelic series of 23 resistance genes, the original M1-a12, and 22 mutant genes, ranging in infection type from 0 and gradually up to 3-4 cn. Further, the race specificity of the 23 allelic genes being the same imply that the 23 resistance genes have one and the same matching avirulence gene in the pathogen.

It should also be pointed out that one of the inherent characteristics of gene M1-a12, the race specificity, has not mutated in any of the above cases, whereas the other characteristic, the infection type, has mutated quite frequently. One interpretation is that gene M1-a12 has two "functions", one recognizing the avirulent pathogen, and the other determining quantitatively the phenotypic expression of resistance. The latter function is probably a question of amount of gene product, because M1-a12 is semi-dominant, and the mutants represent grades on the same scale.

The third main result deals with the last three mutants, M22, M82, and M100, that have infection types 2-3 nc, 1-2 nc, and 2-3 nc, respectively. M22 has a semi-dominant mutant gene inherited independently from gene M1-a12 on which it acts by changing the infection type of M1-a12 homozygous from 0 to 0-1 n and 1-2 on, respectively, when the mutant gene is heterozygous and homozygous. The mutant gene changes the infection type of M1-a12 heterozygotes from 1-2 on to 2-3 on and 4, respectively, when the mutant gene is heterozygous and homozygous. The other two mutants, M82 and M100, have each a recessive mutant gene inherited independently from gene M1-a12 on which they act by changing the infection type of M1-a12homozygotes from 0 to 1-2 on and 2-3 on, respectively. The infection type of M1-a12 heterozygotes are changed from 1-2 on to 4 by both mutant genes. These data may suggest that the three mutant genes are mutually different. It is likely that they are in different loci.

The three mutant genes that affect the low infection type of gene M1-a12 imply that the mother line 'Sultan-5' must have at least three genes in "wild-type" loci the function of which is essential for the usual, full expression of resistance gene M1-a12. If these genes are partly or completely inactivated by mutation, the resistance conferred by M1-a12 is "suppressed". It is tempting to believe that the - possibly three - loci harbouring the "suppressor" mutant genes are involved in the actual resistance mechanism leading to the phenotype we observe and describe as infection type.

One interpretation of the above results suggests that the complete sequence of genetic events begins with the avirulence gene product from the pathogen being recognized by resistance gene M1-a12. Gene M1-a12 is then "induced" to produce a gene product, which quantitatively regulates the activity of three or more structural genes. These genes may produce the actual compounds that result in the hypersensitive death of the host cells challenged or invaded by the pathogen.

References:

Torp, J. and J. Helms Jørgensen. 1986. Modification of powdery mildew resistance gene M1-a12 by induced mutation. Can. J. Genet. Cytol. 28:725-731.

Jørgensen, J. Helms. 1987. Genetic analysis of mutants for powdery mildew susceptibility in barley (in preparation).