Section 4 — Gene Action 



and on sucrose/sorbose point to a regulatory 

 mechanism related to the (3-galactosidase system 

 in E. coli. The mutants are supposed to be con- 

 stitutive for a sucrose splitting enzyme, which in 

 the wild type can be repressed by sorbose. 



A genetic factor for colonial growth has been 

 crossed into the mutant strains, to check for 

 correlations between the repressor function of 

 sorbose and its ability to induce colonial growth. 



1. De Serres, Kolmark and Brockman, Nature 

 193, 556, 1962. 



4.4.Genetic Studies on ur Mutants of Coprinusradia- 

 tus (Fr. ex. Bolt). Georges Prevost (Gif-sur- 



Yvette, France). 



The species studied is a basidiomycete having 

 dikaryotic phase. This work has been under- 

 taken in order to understand physiological me- 

 chanisms underlging the regulatory systems which 

 occur in dikaryotic organisms. 



Four groups of alleles controlling the bio- 

 synthesis of uracil have been found: ur 1. (Chro- 

 mosome VI), ur 4. (Chr. IV), ur 7. (Chr. VII) and 

 ur 13. (Chr. III). On the other hand a gene r, 

 linked to ur 7 (max. 6 UCO) permits the utili- 

 zation of orotic acid as a source of uracil by 

 strains ur 1. and ur 4. but not by strains ur 7. and 

 ur 13. The gene /- is recessive, which means that 

 the dikaryon (//;■ /. r + ur. 1. r+) cannot utilize 

 orotic acid. The r gene does not control a per- 

 mease system but it permits the participation of 

 orotic acid in the pathway of uracil biosynthesis. 

 The very high sensitivity of the wild type strains 

 to the action of 5-fluorouracil (inhibition of 

 growth by concentration of 10~ 7 m of 5-FU) has 

 led to the utilization of this product for selection 

 of possibly derepressed or/and desinhibited mu- 

 tants. Monogenic mutants resisting to 5-FU 

 (10~ 4 m) have been obtained. These mutants can 

 be classified in several allelic groups and are re- 

 cessive or semi-recessive. Their relationship to 

 mutants ur~ as well as the mechanisms of resist- 

 ance to 5-FU have been analysed. 



4.5. Further Studies with Methionine Mutants of 

 Salmonella typhimurium LT2. D. A. Smith 

 and J. D. Childs (Birmingham, Great Britain). 



The results of growth response, cross-feeding 

 and transduction experiments with 166 mutants 

 suggest that at least 6 genes (met A, B, C, E, F 

 and G) are involved in the synthesis of methionine 



via cystathionine and homocysteine. Met A mu- 

 tants are unable to carry out one, and metB 

 mutants the other, of two successive steps in the 

 synthesis of cystathionine, metC mutants cannot 

 synthesize homocysteine and metE, F and G 

 mutants possess metabolic blocks between homo- 

 cysteine and methionine. MetE mutants have an 

 alternative requirement for vitamin B12. All 

 metC mutants appear to be heat sensitive. 



Colicine mediated genetic transfer results in- 

 dicate the sequence metB — (metF — metE) — met A 

 — metC for 5 of the 6 genes. Only metB and metF 

 are close enough to be transduced by the same 

 phage particle. 



Intragenic abortive and complete transduction 

 tests between all the mutants of each gene are 

 being carried out. Mutants of each of the met A, 

 Fand G genes all fall into single complementation 

 groups. Those of the metB gene fall into at least 

 three and those of metF gene into two groups. 

 The occurrence of suitable met A and F deletion 

 mutants permit some mapping of sites of mutat- 

 ion within these genes. 



4.6. The Gene-Enzyme-Complex Involved In L-arabi- 

 nose Metabolism. Ellis Englesberg, Nancy 

 Lee and Richard Cribbs (Pittsburgh, U.S.A.). 



Forty-seven L-arabinose nonutilizing mutants 

 sites of Escherichia coli, strain B/r, have been or- 

 dered between the markers threonine (thr) and 

 leucine (leu) by transduction experiments with 

 phage Plbt employing three factor crosses. The 

 mutant sites fall into four different gene loci, as 

 defined by both genetic and functional criteria 

 and are arranged in the order thr — D, A, B, 

 C— leu. 



Genes A and B are the structural genes for l- 

 arabinose isomerase L-ribulokinase, respectively. 

 Gene D is probably the structural gene for l- 

 ribulose-5-phosphate-4-emimerase. Gene C is 

 characterized by mutants which are deficient in 

 all three enzymes. Recent experiments (Helling, 

 Weinberg, and Englesberg, unpublished), con- 

 ducted with K12, using temporary merozygotes, 

 have shown that C mutants complement both 

 A and B mutants thereby eliminating the possi- 

 bility, previously considered, that C is an operator 

 locus. Mutations in the B gene have a dual effect 

 causing alterations in the structure of the kinase 

 and increased or decreased inducible levels of 

 isomerase and epimerase. The mutant sites 

 affecting high and low inducible levels of these 

 two enzymes are distributed in a random fashion. 

 The amount of inducible L-ribulokinase CRM 

 formed by some B gene mutants is greater or less 

 than the amount of L-ribulokinase (as deter- 



38 



