At the apogee of the early phage school, Luria & Human (1952) made a remarkable observation: phage T2, grown on a strain of coli B/4, was unable to go through a second growth cycle on the same host (as shown much later, the critical step lay in traversing the host cell membrane). Only a special strain of Shigella dysenteriae would permit growth of these phages; however, the descendants from the growth cycle in Shigella could grow again on B/4. It looked as though the phages coming out of B/4 could remember their last host; they were somehow modified by it, marked. This example brought to light the phenomenon of host-dependent modification (M), which cried out for an explanation. This observation described by Luria & Human turned out to be quite a special case, based on the incapacity of the strain E. coli B/4 to synthesize uridine-diphosphoglucose (UDPG), a compound necessary for the typical glucosylation of T2 DNA. The glucosylation of T2 DNA was a prerequisite for its penetrating through the cell membrane of E. coli; this, because a DNAase located there (absent in Shigella), broke down the unglucosylated T2 DNA. The phage T2 was thus “restricted” in its growth; in other words, it was subjected to the phenomenon of restriction (R) by this particular strain of coli. This peculiar occurrence was — and still remains — a typical instance of the matters preoccupying researchers confined in their academic ivory towers. Many further restricting and modifying hosts, as well as restricted and modified phages, were discovered; one special case was scrutinized by Werner Arber and his co-workers at the University of Geneva (see, for instance, Arber, 1965a, 1968; Arber & Linn, 1969):
KeywordsHaemophilus Influenzae Host Cell Membrane Shigella Dysenteriae Phage Titre Single Restriction Enzyme
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