CHROMOSOME LOCALIZATION OF GENES FOR RESISTANCE TO HETERODERA-SCHACHTII, CERCOSPORA-BETICOLA AND POLYMYXA-BETAE USING SETS OF BETA-PROCUMBENS AND BETA-PATELLARIS DERIVED MONOSOMIC ADDITIONS IN BETA-VULGARIS
M. Mesbah et al., CHROMOSOME LOCALIZATION OF GENES FOR RESISTANCE TO HETERODERA-SCHACHTII, CERCOSPORA-BETICOLA AND POLYMYXA-BETAE USING SETS OF BETA-PROCUMBENS AND BETA-PATELLARIS DERIVED MONOSOMIC ADDITIONS IN BETA-VULGARIS, Euphytica, 97(1), 1997, pp. 117-127
Beet cyst nematodes (BCN, Heterodera schachtii), Cercospora beticola,
and rhizomania, caused by the beet necrotic yellow vein virus (BNYVV)
and vectored by the soil-borne fungus Polymyxa betae, are the most ser
ious diseases of sugar beet (Beta vulgaris subsp. vulgaris). The wild
Beta species of section Procumbentes are known to be completely resist
ant to H. schachtii, C. beticola and P. betae. Alien monosomic additio
ns (2n=19), plants of cultivated beet (2n=18) carrying different indiv
idual chromosomes of B. procumbens (2n=18) or B. patellaris (2n=36), w
ere tested in greenhouse experiments for resistance to these pathogens
. Gens(s) conferring full resistance to the beer cyst nematode in B. p
atellaris are located on chromosome 1.1, and the other tested chromoso
mes of B. patellar-is are not involved in the expression of resistance
. Artificial inoculation under greenhouse conditions, with in vitro pr
oduced inoculum of C. beticola and spot-percentage rating of the disea
se intensity, showed that the high level of resistance that was observ
ed in the wild species B. procumbens and B. patellaris was not found i
n any of the monosomic additions tested. It was suggested that genes o
n various chromosomes of the wild species are needed to express full r
esistance, and that the chromosomes of group 7 of B. patellaris and ch
romosome 7 of B. procumbens have the largest effect. The greenhouse te
sts for resistance to P. betae in B. patellaris derived monosomic addi
tions showed that the addition families of group 4.1 have a strong par
tial resistance, while the addition families of group 8.1 appeared to
be completely resistant to the pathogen. Resistance to P. betae in the
two wild species as well as in the two resistant addition types did n
ot exclude infection with BNYVV, but resulted in a considerable reduct
ion of the virus concentration. It was concluded that resistance to th
e vector would complement virus resistance, and may provide a more eff
ective and durable control of rhizomania.