Worm Breeder's Gazette 10(2): 151

These abstracts should not be cited in bibliographies. Material contained herein should be treated as personal communication and should be cited as such only with the consent of the author.

Ultraviolet Mutagenesis and Effects of rad-1, 3, & 7

Thomas Coohill, Tamara Marshall, Wayne Schubert and Gregory Nelson

Figure 1

Figure 2

Four tester strains of worms are being used to characterize 
mutagenesis as a function of different classes of radiation including: 
UV, gamma / X-rays, and ionizing particles.  The strains employ the 
eT1 balancer technique first introduced by Rosenbluth and Baillie.  
Here we report results for UV 254 nm lethal mutant induction.  The 
four strains utilized have the following genotypes: [See Figure 
1]
Worms were irradiated as young adults on the surfaces of unseeded 
NGM plates and transferred to seeded plates to expel embryos in utero 
during irradiation followed by a transfer to clean plates for egg 
laying.  10 F1's per P0 were scored for failure to segregate Dpy-18;
Unc-46's indicating the presence of at least one lethal in the eT1 
balanced region.  291 - 691 F1's were scored per condition.  UV 
conditions were: one GE 15T8 germicidal lamp at 40 cm from the plate 
surface giving a flux of 1 Watt/m2 and exposures were verified with a 
UV photometer.  The results are given in the accompanying figures.  
They show that the exposure vs response rises to a plateau at 4.5 to 
5% mutants per 40 map units.  (For UV mutageneses, in general, a 
suggested exposure is therefore 150-175 Jm-2).  This saturating 
behavior is not unlike bacterial or mammalian cell responses (Harm, W.,
Biological Effects of Ultraviolet Radiation, Cambridge U.  Press, 
1980).  A rough calculation suggests that the response is probably 
largely due to sperm as oocytes are substantially shielded by 
overlying tissue.  When rad-x mutations are present in the strains, 
hyper and hypo mutability are observed.  rad-3 is the most UV-
sensitive of the known rad mutants and exhibits a high mutation rate 
even at the very low fluence of 5 Jm 2.  rad-1 and rad-7 reduce the 
mutability.  A convenient interpretation would be that hypermutability 
occurs when lesions can only be processed by an error prone repair 
system whereas hypomutability occurs when damage is repaired in an 
error free manner and that repair proceeds along a branched pathway.  
Preliminary data suggest that rad-7 may be hypermutable to gamma ray 
and ion damage.
[See Figure 
2]

Figure 1

Figure 2