Brassinosteroids (BRs) play important roles throughout plant development. A
lthough many genes have been identified that are involved in BR biosynthesi
s, genetic approaches in Arabidopsis have led to the identification of only
one gene, BRI1, that encodes a membrane receptor for BRs. To expand our kn
owledge of the molecular mechanism(s) of plant steroid signaling, we analyz
ed many dwarf and semidwarf mutants collected from our previous genetic scr
eens and identified a semidwarf mutant that showed little response to exoge
nous BR treatments. Genetic analysis of the bin2 (BR-INSENSITIVE 2) mutant
indicated that the BR-insensitive dwarf phenotype was due to a semidominant
mutation in the BIN2 gene that mapped to the middle of chromosome IV betwe
en the markers CH42 and AG. A direct screening for similar semidwarf mutant
s resulted in the identification of a second allele of the BIN2 gene. Despi
te some novel phenotypes observed with the bin2/+ mutants, the homozygous b
in2 mutants were almost identical to the well-characterized bri1 mutants th
at are defective in BR perception. In addition to the BR-insensitive dwarf
phenotype, bin2 mutants exhibited BR insensitivity when assayed for root gr
owth inhibition and feedback inhibition of CPD gene expression. Furthermore
, bin2 mutants displayed an abscisic acid-hypersensitive phenotype that is
sh a-red by the bri1 and BR-deficient mutants. A gene dosage experiment usi
ng triploid plants suggested that the bin2 phenotypes were likely caused by
either neomorphic or hypermorphic gain-of-function mutations in the BIN2 g
ene. Thus, the two bin2 mutations define a novel genetic locus whose gene p
roduct might play a role irt BR signaling.