The ultraviolet resistance of a streptolydigin-susceptible strain of Escherichia coli B/r hcr(-) increased during preirradiation treatment with streptolydigin (an inhibitor of deoxyribonucleic acid-dependent ribonucleic acid polymerase) for 20 min and then remained constant. During preirradiation treatment with chloramphenicol (an inhibitor of protein synthesis), resistance to ultraviolet light increased for 1 to 2 h, and reached a maximal level significantly above that attained in streptolydigin-containing medium. These results suggest that there are two mechanisms that function in Hcr(-) cells during chloramphenicol treatment which contribute to the concomitant ultraviolet resistance enhancement. One is ribonucleic acid dependent and is inhibited by streptolydigin. This ribonucleic acid-dependent mechanism appears to be absent in wild-type and RecA E. coli B/r strains.