ISSN:
1617-4623
Source:
Springer Online Journal Archives 1860-2000
Topics:
Biology
Notes:
Summary Expression of the P RE (establishment) pathway for λ repressor synthesis is regulated both by phage-specific genetic elements and by physiological conditions. Here we describe the effects of temperature, multiplicity of infection, mutations in the cro gene, and a mutation in P RM on P RE-directed repressor synthesis. As Reichardt (1975a) has shown, repressor synthesis begins 5–15 min after infection by λ wildtype phage, and is shut off at 20–30 min after infection, depending on the temperature. At 43°, synthesis starts sooner, shuts off earlier, and leads to lower repressor levels than are attained at lower temperatures. Experiments with the temperature sensitive mutant crots20 demonstrate that, as had been shown previously in experiments at 30° and 37° C, cro protein is responsible for the shut-off of repressor synthesis at 43°. In addition to the effects of temperature, the kinetics of repressor synthesis are strongly affected by multiplicity of infection (moi). At mois greater than 10, repressor synthesis after infection by λ wildtype at 30° is dramatically inhibited. Unexpectedly, the P RM mutation prm116, under certain conditions, can alleviate both cro-mediated shutoff and the inhibition of P RE-directed repressor synthesis at high moi. These effects of prm116 are observed only at low temperature (30°–32° C) and at mois of about 6–10 or greater; they also appear to be cis-specific. Possible mechanisms for the effects of the prm116 mutation are discussed. Finally, these studies demonstrate that crots20, which was isolated as a temperature-sensitive lethal mutation in the cro gene (Herskowitz, unpublished), is temperature-sensitive with respect to the ability to shutoff P RE-directed repressor synthesis; however, even at low temperature (30° C), the crots20 gene product is only partially active.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1007/BF00425472
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