Worm Breeder's Gazette 9(1): 46

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.

Caffeine-resistant mutants of C. elegans

P. Hartman and R. Donlon

Wild-type animals largely arrest development if L1's are placed on 
NG plates containing 30 mM or greater concentrations of the 
methylxanthin-derivative caffeine.  Eleven mutants have been isolated 
among the F2 progeny of EMS-mutagenized animals in which this 
developmental delay is less severe.  Although caffeine delays 
development in these mutants, most attain adulthood and produce 
progeny.  Wild-type and mutant L1's have been incubated on plates 
containing between 5mM and 40mM caffeine and their lengths measured 
after three days.  Increasing caffeine concentrations reduced length 
in a roughly linear fashion.  All eleven mutant strains were 
approximately as resistant as N2, as judged by this criterion.  The 
mutations are recessive and define two new genes, named caf-1 and caf-
2.  There are eight alleles of caf-1 and three alleles of caf-2.
Linkage testing shows caf-1 is on LGII.  It is left of dpy-10 as 
indicated by a 3F cross using dpy-10 and unc-4.  Two factor crosses 
place it 39 mu away from unc-4 and 21 mu away from sqt-2.  You LGII 
fanatics realize that this is way out in left field.  The second gene 
is right of unc-13, as indicated by a 3F cross using dpy-5 and unc-13.  
A 2F cross places it approximately 6.7 mu right of dpy-5.  This agrees 
well with observation that caf-2/nDf24 heterozygotes are resistant to 
caffeine.
Caffeine-resistant strains of Escherichia coli are often altered in 
their lethal responses to UV and ionizing radiations (Grigg, 1967.  
Mutat.  Res.  4, 553; Delvaux and Devoret, 1969.  Mutat.  Res.  7, 273)
.  It was hoped a similar situation would exist with C.  elegans, thus 
providing a selection for additional rad mutants.  Preliminary 
inactivation data suggest that this is not the case.  We hope to 
further characterize the mutants by: 1) assaying sensitivities to 
other methylaxanthin derivatives, including theophylline; 2) 
constructing a caf-1; utant and determining 
its sensitivities; and 3) testing for suppression of all alleles by 
sup-7; and 4) assaying for metabolism of caffeine in N2 and the caf 
mutants.  Suggestions for additional experiments are most welcome.