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Biomedical subjects

J Weil

Publications and source records attributed to J Weil.

At least 145 records · Page 8Linked to original sources
PubMed1976

Characterization of T4 mutants that partially suppress the inability of T4rII to grow in Lambda lysogens.

In the course of isolating viable T4 deletions that affect plaque morphology (HOMYK and WEIL 1974), two closely linked point mutant, sip1 and sip2, were obtained. They map between genes t and 52, cause a reduction in plaque size and burst size, and partially suppress the lethality of rII mutants for growth in lambda lysogens. The characteristics demonstrate that sip1 and sip2 are similar to mutants previously reported by FREEDMAN and BRENNER(1972). In addition, D. Hall (personal communication) has shown that sip1 and sip2 are similar to the mutant farP85, which affects the regulation of a number of early genes (Chace and Hall 1975).--Sip suppression of rII mutants can be demonstrated in one-step growth experiments, even when both rII genes are completely deleted. This indicates that sip mutants do not simply reduce the level of rII gene products required for growth in a lambda lysogen. Instead, they alter the growth cycle so as to partially circumvent the need for any rII products.--Mutations at two other sites, designated L1 and L2, reverse the poor phage growth caused by sip and, in the one case tested, reverse the rII-suppressing ability of sip.

Chromosome Deletion↗
PubMed1975

Recombination-deficient deletions in bacteriophage lambda and their interaction with chi mutations.

We have isolated a new class of deletion mutants of phage lambda that extend from the prophage attachment site, att, into the gam and cIII genes. In this respect they are similar to certain of the lambda pbio transducing phage, but they differ in having a low burst size and in forming minute plaques. Lytically grown stocks of the deletions contain a variable proportion of phage that produce large plaques. These have been shown to carry an additional point mutation. Similar mutations, called chi, have been described by Lam et al. (1974), who showed that they result in a hot-spot for recombination produced by the host recombination system (Rec). We show that chi mutations can occurat several sites in the lambda genome and produce a Rec-dependent increase in the burst size of the one deletion tested.---In addition to reducing burst size, the one deletion tested reduces synthesis of DNA and emdolysin but increases production of serum blocking protein. A chi mutation partially restores DNA synthesis and endolysin production and reduces serum blocking protein to normal levels. Our results are consistent with the hypothesis put forward by Lam et al., that chi enhances the frequency of Rec-promoted recombination, which provides the only pathway for production of maturable DNAin a red gam infection. The mechanism of the differential effect on protein production is, however, unclear.---Chi mutations are found to occur in DNA other than that of lambda. We show that, as has been suggested elsewhere (McMilin, Stahl and Stahy 1974), the lambda pbio transducing phages carry a chi mutation within the E. coli DNA substitution. A chi mutation also arose in a new substitution of unknown origin isolated in the course of this work.

Chromosome Aberrations↗