Evidence for the Genetic Control of Photoreactivation1

HOTOREACTIVATION is the reversal by near-ultraviolet or visible light of 'ultraviolet radiation damage to biological systems ( JAGGER 1958). This phenomenon has been demonstrated in the intact cell in a spectrum of organisms (extending from bacteria to mammals) (JAGGER 1958) and in vitro with ultravioletinactivated transforming factor (deoxyribose nucleic acid) of Hemophilus in@uenzae ( GOODGAL, RUPERT, and HERRIOTT 1957; RUPERT, GOODGAL, and HERRIOTT 1958). Photoreactivation of the above factor following ultraviolet treatment proceeds only in the presence of cell-free extracts which thus far may be obtained from either Escherichia coli (RUPERT et al. 1958) or baker's yeast (RUPERT, in press). The activity of these extracts resides in a cellular component, probably an enzyme, present in some organisms while absent in others. One implication of the above in uitro experiments, when coupled with the observed variability or lack of photoreactivation within species or families of microorganisms (BELLAMY and GERMAIN 1955; STUY 1956; GOUCHER and KOCHOLATY 1957; GOODGAL et al. 1957), is that the photoreactivation mechanism in the intact organism is under genetic control. Direct evidence for the genetic control of photoreactivation is presented in the present study on the photoreactivation of ultraviolet-induced extrachromosomal mutations (producing respiratory deficiency) in yeast. Genetic nomenclature of ultrauiolet-induced respiration deficient mutants: The induction of respiration deficient mutants of yeast by ultraviolet and the photoreactivation of this mutation have been previously described (RAUT 1954; PITTM A N 1956; SARACHEK 1958; PITTMAN, RANGANATHAN, and WILSON 1959). These mutants are phenotypically similar to spontaneously derived respiration deficient variants in their inability to (1) consume significant quantities of oxygen (WHELTON and PHAFF 1947), ( 2 ) grow on an obligate aerobic substrate such as lactate (OGUR and ST. JOHN 1956), and (3) reduce triphenyl tetrazolium chloride (OGUR, ST. JOHN, and NAGAI 1957). Genetic analyses (RAUT 1954; PITTMAN 1959) show that the majority (about 95 percent) of respiration deficient mutants derived from ultraviolet irradiated haploid stocks fall into three classes, each having been previously described by EPHRUSSI and co-workers ( CHEN, EPHRUSSI, and HOTTINGUER 1950; EPHRUSSI 1953) : (1) petite mutants, the principal class, which result from the loss or functional inactivation of extrachromosomal determinants; (2) genic (or segregational) mutants which carry the recessive allele of a gene controlling respiration; and (3) double mutants