0
$\begingroup$

In the paper that introduced TRANSDUCTION (J Bacteriol. 1952 Nov;64(5):679-699), Lederberg and his student Zinder reported that S. typhimurium

"LT-22 is lysogenic for a virus active on LT-2. This virus is capable of inducing lysogeny in LT-2."

I read this line as: LT-22 carries a prophage that, upon induction, can infect LT-2.

They then used subsets of these strains: LA-2 (also known as SW-414), which required methionine and histidine; and LA-22, a collection of strains with different metabolic requirements.

Zinder and Lederberg commented that

Prototrophs appeared in the platings of LA-22 but not of LA-2. Sterile filtrates of LA-2 broth cultures did not elicit prototrophs from LA-22. However, filtrates from mixed cultures of LA-2 and LA-22 elicited about one prototroph per million LA-22 cells. Thus LA-2 produced a filtrable agent (FA), under stimulation from LA-22, that could elicit prototrophs from LA-22. Filtrates of LA-22 cultures, containing substantial amounts of phage (PLT-22) active on LA-2, also stimulated FA production from LA-2.

Thus, LA-2 produced a phage that infected LA-22 to produce a prototroph.

But if the phage was present in LA-22 (derived from LT-22), how could it infect LA-2 (derived from LT-2)?

Is there a detailed explanation of this experiment?

Thank you

$\endgroup$
2
  • $\begingroup$ Regarding the bolded sentence, it's not surprising that a prophage from one strain of salmonella would infect another salmonella strain. What part of the process needs explanation? $\endgroup$
    – timeskull
    Commented Feb 5 at 18:35
  • $\begingroup$ The fact that the phage moved from LA-22 to LA-2, took some genes from it and then re-infected LA-22 (which, being lysogenic for the phage, should have been immune to it) $\endgroup$
    – Gigiux
    Commented Feb 7 at 7:09

1 Answer 1

1
$\begingroup$

There certainly are detailed explanations of the experiments. For this answer I'm using a 2016 retrospective in J. Bacteriology, the same journal that published the original paper. However those descriptions will tend to gloss over the points that concern you as described in your comment:

The fact that the phage moved from LA-22 to LA-2, took some genes from it and then re-infected LA-22 (which, being lysogenic for the phage, should have been immune to it)

Remember, these experiments took place in a very early time for biochemistry. The Hershey-Chase paper that established nucleic acid, not protein, as the carrier of genes was also published in 1952! The "how" of transduction wasn't worked out until later.

The Filterable Agent responsible for transduction between LT-2 and LT-22 is now known as phage P22. Its prophage tends to be integrated into the host genome. When it switches from lysogenic to lytic phase, it replicates its genome while still integrated into the host.

The headful mechanism fills the first capsid with part of the prophage genome and continues through the adjacent bacterial chromosome for up to seven or more successive capsid headfuls.

So, a significant fraction (about 2%) of the virus particles produced by lytic P22 contain host bacterial DNA and little to no phage DNA.

Why superinfection exclusion (SIE) fails in the LT-22 is an interesting question, but it turns out to not be surprising. P22 has four separate SIE systems, and one, sieA works by binding to and blocking the exit of P22's "ejection proteins", so it can stop transduction by preventing entry of any kind of DNA. However, it looks like this system doesn't perfectly prevent DNA injection. From a 1971 paper on P22 SIE:

The frequency of transduction of wild-type lysogens is reduced by a factor of 250, indicating that transducing particles are excluded by P22 prophage

So, if the concentration of P22 particles with bacterial DNA is high enough, a few will get through.

Incidentally, I found that LT-2 was first isolated in Sweden, and LT-22 in Chile, both in the 1940s.

$\endgroup$
5
  • 1
    $\begingroup$ Thank you, I also read that paper. Your answer gives a better understanding of the issue. Tx $\endgroup$
    – Gigiux
    Commented Feb 8 at 9:49
  • $\begingroup$ I hav found more info in two more papers. In Microbiol Rev 1978;42:385 it is said: "P22 ... generalized transducing particles consist primarily of host DNA... the transductant carries the transducing material as long as the prophage is present". Thus, lysogeny is actually needed for transduction to occur. $\endgroup$
    – Gigiux
    Commented Feb 10 at 9:01
  • $\begingroup$ In the same paper, P22 superinfection exclusion is described as follows. There are 3 mechanisms (1) "chemical modification of the cell surface component (the 0 antigen)" but " P22 lysogens still adsorb P22 virions, but less efficiently"; (2) "preventing entry of the DNA of superinfecting phages into the cell" but " The sieA exclusion system can be saturated by high multiplicities of infection"; (3) "sieB" which " does not act on wild-type P22". Thus, one can assume either that there were many viruses that saturated sieA or that Zinder used sieA mutants... $\endgroup$
    – Gigiux
    Commented Feb 10 at 9:08
  • $\begingroup$ In both cases, the model is more complicated than that delineated by Zinder himself. $\endgroup$
    – Gigiux
    Commented Feb 10 at 9:09
  • 1
    $\begingroup$ The second paper (doi: 10.1128/mbio.02169-23) indicates 4 mechanisms of P22 superinfection exclusion; which Zinder had to bypass to obtain transduction. The additional one is the C2 repressor, which assures the non-expression of lytic genes (but does not exclude the insertion of new prophages). $\endgroup$
    – Gigiux
    Commented Feb 10 at 9:12

You must log in to answer this question.

Not the answer you're looking for? Browse other questions tagged .