THE ROLE OF AUTOTOXINS FROM ROOT RESIDUES OF THE PREVIOUS CROP IN THEREPLANT DISEASE OF ASPARAGUS

Authors
Citation
Wj. Blok et Gj. Bollen, THE ROLE OF AUTOTOXINS FROM ROOT RESIDUES OF THE PREVIOUS CROP IN THEREPLANT DISEASE OF ASPARAGUS, Netherlands journal of plant pathology, 99, 1993, pp. 29-40
Citations number
29
Categorie Soggetti
Plant Sciences",Agriculture
ISSN journal
00282944
Volume
99
Year of publication
1993
Supplement
3
Pages
29 - 40
Database
ISI
SICI code
0028-2944(1993)99:<29:TROAFR>2.0.ZU;2-J
Abstract
Replant disease is a common phenomenon in asparagus growing in the Net herlands. It is distinct from the decline phenomenon reported from man y other asparagus producing area's. The involvement of autotoxins from root residues of former asparagus crops was evaluated. Residues of as paragus roots decompose extremely slowly. At two locations, each with fields where asparagus production was terminated 1 and 10 years before , biomass of root residues was 4180 and 11060 kg dw ha-1 after 1 year and 420 and 1140 kg dw ha- 1 after 10 years. Although 10-year-old resi dues were for the greater part decomposed, crude aqueous extracts inhi bited root growth of asparagus seedlings significantly and even more o f garden cress. In root observation boxes with field soil mixed with n on-sterilized or sterilized asparagus root fragments, growth of second ary roots was inhibited. Non-sterilized strawberry roots did not inhib it root growth, suggesting that effects of organic matter were not inv olved. In a pot experiment, sterilized asparagus root fragments inhibi ted root growth when added at a rate of 20 g l-1, but not at 2 g l-1. Addition of non-sterilized root fragments strongly inhibited root grow th at both levels. This was probably due to simultaneous infection by Fusarium oxysporum present in these residues. When an asparagus field is replanted, the amount of root residues left behind in soil after te rmination of the crop in the previous season is about 2 g dw l-1, that corresponds to approx. 11000 kg dw ha-1. This level is too low for co nsidering direct growth inhibition by autotoxins as a major factor. Th eir possible indirect effects are briefly discussed.