14 
alleles into )J849 which could be maintained throughout the remainder of 
the construction, and thus be present in )(L776. 
§4. The introduction of the thyA 57 allele by P1L4 transduction 
(which, It is important to note, carried with it an associated unchar- 
acterized thermosensitive mutation, see §2d, above) was not controlled by 
monitoring the cotransduction of a linked marker. This could have been 
accomplished by simply cotransducing the closely linked marker pair 
thyA 57 -lysA 32 (0.3 minutes apart). 
Genotypic characterization : 
§ 5 . sup E4 2 : 
a) The presence of the sup E42 mutation was assayed by the 
+ 
ability of X1776 thr transductants to plate Tcl^ at an e ^fi c i- enc y 
of 10 
-3 
Curtiss et al. conclude from this observation that either 
expression of the supressor has been modified or that the abilities of 
Xvir (control) and ^cl N N to productively infect X1776 thr + 
derivatives differ. Curtiss and co-workers favor the latter hypothesis 
since AcI 0 „N\N _ fails to plaque on glucose-grown cells. However, 
ojJ — / — /IJ 
this phenomenon is well-characterized; lambda adsorbs, as a rule, 
poorly on glucose-grown cells, since its receptor, specified by the malB 
gene is subject to catabolite repression (Maxime Schwartz, personal 
communication). Controls for the relative adsorption efficiencies of 
)y i r and Tel N on maltose-grown versus glucose-grown cells are 
not presented. 
b) Alternative explanations for the observed lowering of 
plating efficiencies of ?cl 0 .N-,N 01 ~ include the possibility that an 
additional phenotype resembling nus (Friedman, 1971) or gro iT 
[Appendix C — 202] 
