“…The tof gene product prevents repressor synthesis during the lytic cycle. But during the lysogenic cycle the reverse is true: the repressor prevents expression of the tof gene (4)(5)(6). In the system we are studying, we have discovered that the regulatory gene makes a repressor which represses its own synthesis, in addition to repressing the synthesis of the enzymes of the system.…”
The enzymes mediating histidine utilization, coded by the hut genes, in Salmonella typhimurium -are synthesized from two closely-linked operons. Results presented in this paper show that these operons are regut lated by a single repressor protein. The hutC gene, coding for this repressor, is part of one of the operons. Since this same operon is sensitive to the repressor, the repressor apparently represses its own synthesis.
“…The tof gene product prevents repressor synthesis during the lytic cycle. But during the lysogenic cycle the reverse is true: the repressor prevents expression of the tof gene (4)(5)(6). In the system we are studying, we have discovered that the regulatory gene makes a repressor which represses its own synthesis, in addition to repressing the synthesis of the enzymes of the system.…”
The enzymes mediating histidine utilization, coded by the hut genes, in Salmonella typhimurium -are synthesized from two closely-linked operons. Results presented in this paper show that these operons are regut lated by a single repressor protein. The hutC gene, coding for this repressor, is part of one of the operons. Since this same operon is sensitive to the repressor, the repressor apparently represses its own synthesis.
“…To initiate the expression of desired genes, Rep-operator interactions must be disrupted, which can occur by various means, including the binding of small molecule inducers (2,3). Interactions with these components disrupt the ability of a Rep to bind to the operator by either altering its 3D structure or inducing proteolysis (4).…”
DNA-binding repressors are involved in transcriptional repression in many organisms. Disabling a repressor is a crucial step in activating expression of desired genes. Thus, several mechanisms have been identified for the removal of a stably bound repressor (Rep) from the operator. Here, we describe an uncharacterized mechanism of noncanonical DNA binding and induction by a Rep from the temperate Salmonella phage SPC32H; this mechanism was revealed using the crystal structures of homotetrameric Rep (92–198) and a hetero-octameric complex between the Rep and its antirepressor (Ant). The canonical method of inactivating a repressor is through the competitive binding of the antirepressor to the operator-binding site of the repressor; however, these studies revealed several noncanonical features. First, Ant does not compete for the DNA-binding region of Rep. Instead, the tetrameric Ant binds to the C-terminal domains of two asymmetric Rep dimers. Simultaneously, Ant facilitates the binding of the Rep N-terminal domains to Ant, resulting in the release of two Rep dimers from the bound DNA. Second, the dimer pairs of the N-terminal DNA-binding domains originate from different dimers of a Rep tetramer (trans model). This situation is different from that of other canonical Reps, in which two N-terminal DNA-binding domains from the same dimeric unit form a dimer upon DNA binding (cis model). On the basis of these observations, we propose a noncanonical model for the reversible inactivation of a Rep by an Ant.
“…The loss of immunity is heritable and after prolonged growth at a low temperature only few of the cells become immune (imm +) (Eisen et al, 1968a;Calef and ~eubauer, 1968). It has been suggested that the ere antirepressor present in these lysogens is responsible for this nonimmune (imm-) state Oppenheim et al, 1970;Oppenheim and Slonim, 1971;Calef et al, 1971;Sly et al, 1971;Spiegelman, 1971).…”
Lambda bacteriophage mutants, lambdasar, were isolated. These mutants can form plaques on a non lysogenic lawn and are unable to grow on nonimmune (imm-), cro constitutive hosts. Analysis of the restriction of lambdasar by a set of defective lysogens suggested that both the cro and cII gene products participate in the inhibition. The sar mutations were mapped in the ori region between the genes cII and O. Complementation experiments showed that under the restrictive conditions lamdasar is defective in the expression of both the N and the O genes. Transcription analyses support these findings, as lambdasar is unable to serve as a template for transcription after infecting cro constitutive hosts. In addition lambdasar does not replicate under the restrictive conditions, although its DNA can bind to the host membrane to some extent. The Sar phenotype can be relieved by removing sites of action of cro either by a V2 mutation or by substituting the lambda immunity region by imm434 or imm21. Similarly introducing a cy mutation, which interferes with the action of the cII gene product, also eliminates the Sar effect. The sar mutation can suppress cy mutations as manifested in plaque morphology, lysogenization frequency, cI repressor synthesis and the expression of rex function. Suppression takes place only when the sar mutation is present in cis to cy and it requires the action of the cII and cIII gene products. It is suggested that the sar mutation suppresses cy by activating a new promoter for repressor synthesis, pro. The results also suggest that the cII and cIII gene products may act at a site other than y.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.