Volume 3

Gene expression / Benjamin Lewin.

  • Lewin, Benjamin.
Date:
1974-1977
Catalogue details

Licence: Attribution-NonCommercial 4.0 International (CC BY-NC 4.0)

Credit: Gene expression / Benjamin Lewin. Source: Wellcome Collection.

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    mutants resistant to group I (A) colicins fall into 21 phenotypic classes according to their cross resistance patterns (including those of both the resistant and tolerant types); the mutants resistant to group B colicins fall into 9 such classes. The suggestion that the colicins may fall into two general evolutionary groups also has been made by Hardy, Meynell and Dowman (1973) on the basis of relationships in their abilities to bind to cells. Hardy (1975) has noted that where the plasmid DNA has been isolated, the group I (A) plasmids are small (10 6 -10 7 daltons) whereas the group II (B) plasmids are somewhat larger (about 10 8 daltons); it remains to be seen if this will prove to be a general rule. These and other recent studies make it clear that the distinction be tween resistant and tolerant mutants is less meaningful than had originally been supposed; for both types of mutant may arise in a similar manner. Mutants resistant to a single colicin may indeed represent a specific loss of its receptor protein. However, this cannot be true of mutants resistant to several colicins which bind to different receptors; in this case the mutation must block the presence of all these receptors in the membrane. This latter class of resistant mutant is similar to several previously iso lated classes of tolerant mutant. Among the tolerant mutants charac terized by Nagel de Zwaig and Luria (1967) and by Nomura and Witten (1967) were some classes tolerant only of one colicin, while others were tolerant of different colicins. The second class included the mutations tolll and tolIII which cause changes in the sensitivity of the cell mem brane to disruption by agents such as deoxycholate or EDTA. Many other tolerant and resistant mutants have since been shown to possess altera tions in membrane structure. These include both mutants insusceptible to a single colicin and those refractory to several colicins (Whitney, 1971; Bernstein, Rolfe and Onodera, 1972; Eriksson-Grennberg and Nord strom, 1973; Davies and Reeves, 1975a,b). This suggests that some of the resistant or tolerant mutations result in a change or loss of some component involved in assembly of the cell membrane, with the result that certain colicin receptors either are no longer able to take their place at the surface of the cell (in resistant mutants) or if present are inhibited in their ability to transmit colicin or effector molecules from the receptor site (in tolerant mutants). The spec ificity of the effect of the membrane change can vary very greatly. This interpretation implies that resistance and tolerance should be regarded as related mechanisms that may simply reflect the stage at which action of the colicin is prevented. Each colicin has a characteristic killing action. Colicin K inhibits DNA, RNA, and protein synthesis; inhibition may be prevented by the addition of trypsin after colicin binding to the cell, which argues that the colicin