A mutant strain of Drosophila melanogaster with five markers on the X-chromosome was found to be more sensitive than the wild type when infected with an insect-pathogenic strain of Serratia marcescens. Two of the five mutations in this fly strain, cut and miniature, were found to be responsible for this sensitivity. A double-mutant, with both cut and miniature, was as sensitive to Serratia infection as was the original sensitive Drosophila strain with all five mutations. Recombinant flies with other alleles of cut and miniature were also sensitive. A revertant of cut was found to be less sensitive than the parental flies. Our insect pathogenic strain of Serratia produces several proteases and a chitinase. A bacterial mutant, lacking proteases and chitinase, was found to be less virulent than wild-type bacteria. When pupal shells from resistant and cut-miniature flies were incubated with a mixture of protease and chitinase there was a release of N-acetyl glucosamine, and 50% more material was liberated from pupal shells of sensitive flies. Sensitive flies reared on sucrose infected with Serratia showed bacteria in their hemolymph earlier than wild-type flies. We conclude that Drosophila genes for cut and miniature are associated with the sensitivity to Serratia infection, presumably because the gut peritrophic membrane is more susceptible to bacterial proteases and chitinase.