SummaryGuided by genetic recombination experiments that placed the gene for theDrosophilamemory mutantamnesiacproximal toforkednearcarnation, we screened 7 deficiencies of the proximal X in an effort to more precisely localize theamnesiacmutation. After training with a classical conditioning procedure, two deficiency chromosomes,mal8andmal12, producedamnesiac-like memory deficits inDf/amnflies but not inDf/+ controls. In contrast, themal13,mal10,mal11,16-3-22andDCBIdeficiencies, in combination with eitheramnor + chromosomes, did not produceamnesiacmemory scores. These results indicate that theamnesiacgene lies between the left breakpoint ofmal12(19A1) and the left breakpoint ofmal13(19A1 or A2). This conclusion is supported by the fact thatamnmales carrying the Y-linked X-chromosome duplicationy+Ymal106(which spans 18F4-5 to 20A) produce wild-type learning and memory scores. Finally, the data suggest thatamnesiacis a complete loss of function (amorphic) mutation, becauseamn/amnandamn/Dfflies have similar learning and memory scores.