Published online by Cambridge University Press: 01 June 1998
Different management regimes for 1-year rotational set-aside were tested in three experiments that followed winter wheat and started in autumn 1988–90. The regimes included operations that prevented the establishment of volunteers or allowed them to establish and persist until either spring or summer, and also altered the distribution of debris from the winter wheat that preceded the set-aside. For comparison, treatments in the set-aside year also included winter wheat.
Samples taken in spring from the first test crop showed that there were few significant or consistent effects on leaf diseases of growing the wheat after different set-aside treatments or after winter wheat. There were significant effects of the set-aside treatments on root and stem base diseases but some of the effects, and the apparent absence of others, are not easily reconciled with current understanding of the biology of the pathogens concerned. In summer, eyespot (Pseudocercosporella herpotrichoides) was most severe after winter wheat and least severe after ryegrass. Severity after the other set-aside treatments did not differ significantly. There was more sharp eyespot (Rhizoctonia cerealis) in plots that had been ploughed at the start of the set-aside year, including those sown with winter wheat, than in those that had not. Brown foot rot (Fusarium spp.) was equally severe where the wheat followed wheat or where it followed set-aside treatments that allowed volunteers to develop, and less so where the development of volunteers was prevented. Take-all (Gaeumannomyces graminis var. tritici) was most severe after winter wheat and more severe after set-aside treatments that allowed volunteers to develop and survive through the winter than after those that did not. Effects of ryegrass (Lolium perenne ssp. multiflorum) on take-all in the following wheat were particularly variable, perhaps because ryegrass is a host of both the take-all fungus and of Phialophora graminicola, one of its principal antagonists.