SummaryTwo mutant lines of barley, Risù 17 and Notch-2, were found to accumulate phytoglycogen in the grain. Like the sugary mutants of maize and rice, these phytoglycogen-accumulating mutants of barley lack isoamylase activity in the developing endosperm. The mutants were shown to be allelic, and to have lesions in the isoamylase gene, isa1 that account for the absence of this enzyme. As well as causing a reduction in endosperm starch content, the mutations have a profound effect on the structure, number and timing of initiation of starch granules. There are no normal A-type or B-type granules in the mutants. The mutants have a greater number of starch granules per plastid than the wild-type and, particularly in Risù 17, this leads to the appearance of compound starch granules. These results suggest that, as well as suppressing phytoglycogen synthesis, isoamylase in the wild-type endosperm plays a role in determining the number, and hence the form, of starch granules.

Avenacins are antimicrobial triterpene glycosides that are produced by oat (Avena) roots. These compounds confer broadspectrum resistance to soil pathogens. Avenacin A-1, the major avenacin produced by oats, is strongly UV fluorescent and accumulates in root epidermal cells. We previously defined nine loci required for avenacin synthesis, eight of which are clustered. Mutants affected at seven of these (including Saponin-deficient1 [Sad1], the gene for the first committed enzyme in the pathway) have normal root morphology but reduced root fluorescence. In this study, we focus on mutations at the other two loci, Sad3 (also within the gene cluster) and Sad4 (unlinked), which result in stunted root growth, membrane trafficking defects in the root epidermis, and root hair deficiency. While sad3 and sad4 mutants both accumulate the same intermediate, monodeglucosyl avenacin A-1, the effect on avenacin A-1 glucosylation in sad4 mutants is only partial. sad1/sad1 sad3/sad3 and sad1/sad1 sad4/sad4 double mutants have normal root morphology, implying that the accumulation of incompletely glucosylated avenacin A-1 disrupts membrane trafficking and causes degeneration of the epidermis, with consequential effects on root hair formation. Various lines of evidence indicate that these effects are dosage-dependent. The significance of these data for the evolution and maintenance of the avenacin gene cluster is discussed.