VARIATION FOR PATHOGENICITY AMONG ISOLATES OF BEAN COMMON MOSAIC-VIRUS IN AFRICA AND A REINTERPRETATION OF THE GENETIC-RELATIONSHIP BETWEENCULTIVARS OF PHASEOLUS-VULGARIS AND PATHOTYPES OF BCMV

Citation
Nj. Spence et Dga. Walkey, VARIATION FOR PATHOGENICITY AMONG ISOLATES OF BEAN COMMON MOSAIC-VIRUS IN AFRICA AND A REINTERPRETATION OF THE GENETIC-RELATIONSHIP BETWEENCULTIVARS OF PHASEOLUS-VULGARIS AND PATHOTYPES OF BCMV, Plant Pathology, 44(3), 1995, pp. 527-546
Citations number
26
Categorie Soggetti
Plant Sciences",Agriculture
Journal title
ISSN journal
00320862
Volume
44
Issue
3
Year of publication
1995
Pages
527 - 546
Database
ISI
SICI code
0032-0862(1995)44:3<527:VFPAIO>2.0.ZU;2-E
Abstract
Bean common mosaic virus (BCMV) isolates were collected from crops of Phaseolus vulgaris (bean) and from wild legume species in 13 African c ountries. Isolates of pathotype VIa from both beans and wild legume sp ecies were predominant in central, eastern and southern Africa. Isolat es of pathotypes I, III, IVa, IVb and Va were also found. Some isolate s did not conform to previously published pathotypes, and therefore re present records of novel pathotypes. The susceptibility of various wil d legume species to BCMV was investigated and isolates of the virus ob tained from Crotalaria incana, Rhynchosia sp., Macroptilium atropurpur eum and Cassia occidentalis (synonym Senna occidentalis) were aphid-tr ansmitted both from P. vulgaris to their original host species and to P. vulgaris. Isolates of BCMV from wild legume species were seed-trans mitted in bean and in several other legume species. The natural occurr ence of BCMV in wild legume species in Africa is probably a significan t factor in the ecology and epidemiology of the virus and possibly the evolution of isolates of the 'A' serotype which induce necrotic react ions in cultivars carrying the I gene for resistance. The occurrence o f viruses other than BCMV from P. vulgaris and other legume hosts is a lso reported. The gene-for-gene model described by Drijfhout (1978) is reinterpreted to explain the variation for pathogenicity, and it is p roposed that there may be genes which control the temperature sensitiv ity of necrosis in combination with the I gene.