Recent work by Marchand et al. (1999) has indicated that one form of loose smut (Ustilago nuda) resistance in barley (Ethiopian accession CI 9973) was quantitatively inherited, using molecular markers. This work was inspired, in part, by the author (Therrien et al. BGN 24:10-11) and prompted a re-examination of our original data. Our original conclusion of a two-gene system for resistance was flawed. Table 1 shows significant linkages over several chromosomes, which is clearly quantitative in nature.

This has several implications. First, it is a good thing to keep old data. Second, it is best to approach data from as many angles as is practical - not the unidirectional thinking we originally placed on this data. Third, the value of an informal publication like BGN is clearly seen as a means of promoting further research as an "ideas pool". And lastly, though certainly not least, these findings have strong implications as to how one handles breeding for disease resistance in barley. Conventional wisdom held that resistance to loose smut was monogenic, or digenic . This is no longer the case. Further, the resistance in CI 9973 is as complete as that conferred by a single gene. There are probably many examples (of quantitatively-inherited disease resistance) in barley that we missed, labelling the observed effects as "oligogenetic". In disease resistance studies where the "classical" ratios for resistant:susceptible don't "fit", we now have the means to determine an alternative through molecular markers and QTLs. We can even use the "classical" approach, viz. physiological marker genes as 'visible' QTLs. It is simply a matter of how one looks at it.

Reference:

Marchand, S.; Jean, M.; Rioux, S.; St. Piere, C.A.; and Belzile, F. 1999. Identification of DNA markers linked to loose smut resistance genes in barley. Genome (In Press).