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In a class of tunicamycin-resistant mutants (tmrA7) of Bacillus subtilis, the production of extracellular a-amylase is increase by about five fold. The tmrA7 characteristics (tunicamycin resistance and hyperproduction of extracellular a-amylase) can be transferred to recipient cells by transformation. In the transformants and the original tmrA7 mutant, typical amplification of the region from 4 kb upstream of the amyE gene to the tmrB gene on the chromosome was detected. The repeating unit, 16 kb in size, repeats tandemly about five and ten times in the mutant and transformants, respectively, and the a-amylase production is proportional to the copy number of the amyE gene. Simultaneous amplification of the tmrB gene, which is responsible for tunicamycin resistance in the multicopy state, and the a-amylase structural gene (amyE) seems to be the cause of the pleiotropy of the tmrA7 mutation.