Genetic markers linked with quantitative trait loci (QTL) may enable i
ndirect selection of complex disease resistance. Construction of separ
ate linkage maps to identify QTL for each complex disease resistance t
rait of common bean (Phaseolus vulgaris L.) is unfeasible, however. We
investigated whether selective mapping could be used to hasten identi
fication of random amplified polymorphic DNA (RAPD) associated with QT
L conditioning bean golden mosaic virus (BGMV) or common bacterial bli
ght (CBB) resistance. The mapping population ('Dorado' x XAN 176) cons
isted of 79 F-5:7 recombinant inbred lines. A bulked segregant analysi
s (BSA) of as few as three individuals and selective genotyping was us
ed. The 101 RAPDs identified between the parents were tested across re
sistant vs. susceptible bulks for BGMV reaction, combined greenhouse (
lean and field reactions to CBB, and pod (greenhouse) reaction to CBB.
Fourteen of 22 RAPDs selectively mapped because they cosegregated amo
ng lines within bulks, were linked with seven of the nine QTL conditio
ning resistance as identified by QTL mapping using all 101 RAPDs. The
two QTL not identified by this approach had minor effects. BSA and sel
ective genotyping required only about one-third the cost and labor of
completely classifying the whole population with each marker and was s
imilarly effective for identifying RAPD markers associated with major-
effect QTL that condition disease resistance in common bean. Two-locus
models (R(2)), for select environments, explained 60% of the phenotyp
ic variation in BGMV reaction, and 65, 58, and 46% of the phenotypic v
ariation in greenhouse-leaf, -pod, and field reactions to CBB. Repulsi
on linkages between QTL for BGMV and CBB may complicate the combinatio
n of resistance alleles for these two traits.