Wild-type Shigella flexneri 2a exhibits insensitivity to coliphage lambda.
This insensitivity is linked to a genetic defect in the malA gene cluster and the bacterium's "smooth" lipopolysaccharide layer, hindering lambda adsorption.
Purpose of the Study:
To investigate the genetic basis of Shigella flexneri 2a's insensitivity to coliphage lambda.
To develop functional Shigella flexneri 2a hosts for coliphage lambda propagation and transduction.
Main Methods:
Repairing the malA lesion in Shigella flexneri 2a to enable expression of the malB-lambdarcp region.
Introducing mutations to induce a "rough" lipopolysaccharide character in Shigella flexneri.
Assessing coliphage lambda adsorption, lysogenization, and transduction capabilities in modified Shigella flexneri hosts.
Main Results:
Repairing the malA defect yielded Shigella flexneri derivatives capable of serving as functional hosts for lambda.
Mutations causing a "rough" lipopolysaccharide phenotype enhanced lambda adsorption.
Lambda propagated on a malA(+) rough Shigella flexneri host showed specific restriction patterns in Escherichia coli strains.
Conclusions:
The malA gene cluster and lipopolysaccharide structure are critical determinants of Shigella flexneri 2a's susceptibility to coliphage lambda.
Modified Shigella flexneri strains can serve as effective hosts for lambda propagation and yield gal(+)-transducing lysates.