

CHAPTER 27 



colicinogenic culture actually produce coli- 

 cins. Colicin is lethal to the bacterium syn 

 thesizing it. but colicinogenic cells which do 

 DOl \ icld colicin are viable and immune when 

 exposed to corresponding colicin. Colicin 

 synthesis can be induced in nearly all cells 

 of a colicinogenic culture after exposure to 

 ultraviolet light, nitrogen mustard, or hydro- 

 gen peroxide. Thus, in several of the prop- 

 erties mentioned, colicinogeny and lysogeny 

 are similar, the col factors behaving in these 

 properties like the prophages of temperate 

 phage. When a strain is both lysogenic and 

 colicinogenic, induction often releases either 

 phage or colicin but not both. 



Bacteria can be protected against colicins 

 via immunity or resistance. A colicinogenic 

 bacterium, although immune to the corre- 

 sponding colicin, can possess receptor sites 

 which make it susceptible to colicins of other 

 groups. Certain other genes confer resist- 

 ance to whole groups of colicins by causing 

 the loss of receptors. 



As noted, colicin K and the O antigen are 

 apparently identical. When the receptor 

 sites for colicins and for virulent phages are 

 studied, in a number of cases colicin and 

 phage are found to share receptor sites; for 

 example, receptor sites are shared by colicin 

 K and #T6; colicin E and ^BF-23; colicin 

 C and <f>T\ or <^>T5. Since virulent phage 

 attach to receptors by means of a protein 

 located at the tip of their tails, colicin and 

 tail-tip protein appear to he very similar. In 

 serological tests, however, colicin and phage 

 sharing a common receptor have not been 

 found to exhibit any cross reaction, and 

 colicinogeny does not confer immunity to 

 infection by a site-sharing phage. When 

 bacteria are exposed to the protein coat, or 

 phage ghost, of 4>T2, all protein synthesis 

 (and possibly that of RNA and DNA, too) 

 is halted. The same effect is produced by 

 colicin. Bacteria, however, may recover 

 after exposure to phage ghosts or to colicin 

 ( if the latter is removed by enzymatic diges- 



tion). Sometimes, virulent phage can kill 

 its host without reproducing; in such cases. 

 the constituent responsible lor lethality is a 

 tail-tip protein. When </>T6 is the killer, the 

 lethal protein has the same X-ray inactiva- 

 tion curve, specificity, and receptor site as 

 colicin K. 



Since the lethal protein of T6 is very simi- 

 lar to colicin K. it seems reasonable that T6 

 and col K are homologous with respect to at 

 least one gene. Col K can be thought of as 

 a virulent phage missing that portion of the 

 genome required to lyse the cell and to give 

 rise to particles whose infectivity is inde- 

 pendent of conjugation, yet with enough of 

 the phage genome persisting to make the cell 

 colicinogenic. Labeling experiments show 

 that three col factors studied contained DNA 

 in the amount of 4 to 7 times 10' nucleotide 

 pairs — about one-tenth the amount in F or 

 phage. 



During conjugation, E. coli F + cells trans- 

 fer col El with high frequency, so that col 

 El can exist autonomously. Autonomous 

 col factors can arrive in the F~ cell as early 

 as 2U minutes after conjugation is initiated. 

 Since Hfr E. coli carrying col V, col I, or col 

 E2 do not transfer them in linkage, these col 

 factors give no evidence for an attached state. 



In Salmonella, col I in the absence of F is 

 transferable via conjugation. Although cells 

 carrying only col El cannot transfer it during 

 conjugation, col El cells infected by col I 

 transfer both col factors. Consequently, col 

 I promotes the transfer of col El. When 

 Salmonella harbors only col I, transfer of the 

 chromosome in conjugation occurs but is 

 rare. When such cells are also infected with 

 col El, chromosome transfer increases one 

 hundredfold. As a result, in Salmonella col 

 I promotes the transfer of col El, and col El 

 promotes the transfer of the chromosome. 

 Col I is, therefore, a sex factor. Although 

 they do not cure colicinogeny, acridine dyes 

 inhibit the transfer of col factors. 



When F col~ is crossed with F~ col I, 



