Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:Q9UIJ5 (Rec)
 58,342 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Derivatives of bacteriophage Mu carrying a lac operon and a selectable drug resistance element (Mu d phages) are frequently used tools of bacterial genetics. Mu d prophages used in this way can be treated as transposons, in that the inserted material can be transduced from one strain to another by general transducing phages, such as P1 and P22. When a Mu d prophage is transduced into a new recipient by P1 or P22, the Mu d element can transpose from the transduced fragment into the bacterial chromosome. Transposition of the Mu d element from a P22-transduced fragment shows several striking differences from transposition of a Mu d genome injected by a Mu virion. First, the frequency of transposition from a transduced fragment is greatly enhanced by a P22 helper genome. Second, transposition requires the host recA, B, and C functions. Transposition of Mu following injection by a Mu virion is rec independent. While the basis of these observations is not understood, we suggest that the Mu X protein, a 65-kilodalton protein injected by a Mu virion and required for Mu transposition, may not be packaged by P22. We suggest that the effects seen reflect the behavior of a Mu genome in the absence of the X protein.
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PMID:Rec dependence of mu transposition from P22-transduced fragments. 294 99

Phage P22 can integrate as prophage into a recombination-deficient (Rec(-)) strain of Salmonella typhimurium. At 37 C, the integration efficiency is only 10% that in Rec(+) infection, but at 25 C the efficiencies in Rec(-) and Rec(+) hosts are similar. Rec(-) lysogens cannot be induced by ultraviolet irradiation or by treatments with the chemical inducing agents streptonigrin or mitomycin C. Heat induction of Rec(-) cells lysogenic for a temperature-sensitive c(2) mutant (ts c(2)) is normal, showing that the Rec(-) cell has the machinery necessary for prophage excision. Ultraviolet irradiation of Rec(-) (ts c(2)) lysogens prior to heat induction does not prevent the formation of infective centers after temperature shift. Thus, the noninducibility of Rec(-) lysogens is not due to destruction of the prophage as a result of ultraviolet irradiation. Deoxyribonucleic acid-ribonucleic acid (RNA) hybridization experiments demonstrate that no increase in phage-specific RNA synthesis occurs after ultraviolet irradiation of a Rec(-) (c(+)) lysogen. The Rec(-) mutant appears to lack part of the mechanism required to destroy the phage repressor and allow the initiation of early phage functions such as messenger RNA synthesis. A similar conclusion was reached previously for an Escherichia coli Rec(-) strain.
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PMID:Integration and induction of phage P22 in a recombination-deficient mutant of Salmonella typhimurium. 488 70

Derivatives of P22 with deletions of DNA sequences around and including the erf gene were obtained by crossing phages with plasmids containing fragments of the P22 chromosome. In some cases, the parent phages carried a large insertion in sequences not borne by the plasmids. In these cases, deletion of DNA from the phage chromosome to restore terminal repetition (a selectable trait) could be accomplished by recombination between phage and plasmid DNA in chosen sequences flanking the insertion on both sides and borne by the plasmid. In other cases, the parent phages had deletions of a selectable gene, which could be acquired from the plasmid parents only by acquisition of an overlapping deletion. Deletion-bearing P22 strains were tested for growth and homologous genetic recombination in wild-type, recA-, and rec(B or C)- hosts. This analysis indicated the existence of a gene, mapping to the left of erf, that is helpful (but not completely essential) for growth of P22 in a wild-type host. Because P22 lacking this gene grows as well as wild-type P22 on a recBC- host, it has been designated abc (anti-recBC). The abc gene does not appear to be essential for homologous genetic recombination in any host. A plasmid bearing a 1900 base pair fragment of P22 DNA, that expresses erf and abc under the control of the E. coli lac promoter, was constructed. It supports growth and recombination in a recA- host by a phage that lacks all of the genes known to lie between 24 and 9.
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PMID:Genetic analysis of the erf region of the bacteriophage P22 chromosome. 636 66

Recombinant plasmids having PstI fragments of P22 DNA inserted in the vector pBR322 can be transduced efficiently by Salmonella phage P22, irrespective of the cloned phage sequences. When the rec function of the donor cells and the corresponding recombination system erf of the infecting phage are simultaneously inactivated, only plasmids containing the P22 pac site can be transduced. By this selective, generalized transduction an EcoRV DNA fragment of the P22 related phage L has been identified that carries a base sequence recognized by phage P22 as a packaging signal. Experiments in which only one of the two recombination systems was inactivated, showed that the bacterial rec system obviously promotes cointegrate formation between plasmid and phage DNA much more efficiently than the phage-coded erf system, allowing the specialized plasmid transduction observed by Orbach and Jackson (1982).
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PMID:Selective transduction of recombinant plasmids with cloned pac sites by Salmonella phage P22. 659 17

The transposable tetracycline resistance element, Tn10, can serve as a region of homology to promote rec-dependent deletion, duplication and directed transposition of bacterial genes. Tn10 insertions in regions of the chromosome near the histidine operon (his) have been isolated and characterized in Salmonella typhimurium. When strains are constructed containing two Tn10 insertions flanking the his operon in the same orientation (Tn10-his-Tn10), recombination can occur between Tn10 sequences resulting in the deletion of the intervening his region. The sites of the Tn10 insertions determine the endpoints of the deletion. In crosses designed to construct strains carrying Tn10-his-Tn10, another class of unstable recombinants arises in which the his region exists in tandem duplication, with a Tn10 insertion joining the duplicated copies (his-Tn10-his). The sites of the parental Tn10 insertions mark the endpoints of the duplication. When a strain carrying Tn10-his-Tn10 is used as a donor of his(+) in conjugation or P22-mediated transduction, recombinants can arise in which the his region has been transposed to the site of any Tn10 insertion, far from the normal location of his in the recipient chromosome. In this manner, the his operon has been moved to the site of a pyrB::Tn10 insertion and has been placed on F' plasmids. At these new locations, the his(+) character shows the rec-dependent deletion of his(+) expected for a Tn10-his-Tn10 duplication. These methods should be generally useful for the manipulation of bacterial genes.
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PMID:Abstracts of papers presented at the 1980 meetings of the Genetic Society of America. Boulder, Colorado August 18-20, 1980. 739 62

Under several circumstances, the frequency with which Mud prophages form lysogens is apparently reduced in rec strains of Salmonella typhimurium. Lysogen formation by a MudI genome (37 kb) injected by a Mu virion is unaffected by a host rec mutation. However when the same MudI phage is injected by a phage P22 virion, lysogeny is reduced in a recA or recB mutant host. A host rec mutation reduces the lysogenization of mini-Mu phages injected by either Mu or P22 virions. When lysogen frequency is reduced by a host rec mutation, the surviving lysogens show an increased probability of carrying a deletion adjacent to the Mud insertion site. We propose that the rec effects seen are due to a failure of conservative Mu transposition. Replicative Mud transposition from a linear fragment causes a break in the host chromosome with a Mu prophage at both broken ends. These breaks are lethal unless repaired; repair can be achieved by Rec functions acting on the repeated Mu sequences or by secondary transposition events. In a normal Mu infection, the initial transposition from the injected fragment is conservative and does not break the chromosome. To account for the conditions under which rec effects are seen, we propose that conservative transposition of Mu depends on a protein that must be injected with the DNA. This protein can be injected by Mu but not by P22 virions. Injection or function of the protein may depend on its association with a particular Mu DNA sequence that is present and properly positioned in Mu capsids containing full-sized Mu or MudI genomes; this sequence may be lacking or abnormally positioned in the mini-Mud phages tested.
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PMID:Lethal transposition of Mud phages in Rec- strains of Salmonella typhimurium. 841 85

We have evaluated the diagnostic utility of eleven Toxoplasma gondii recombinant antigens (P22 [SAG2], P24 [GRA1], P25, P28 [GRA2], P29 [GRA7], P30 [SAG1], P35, P41 [GRA4], P54 [ROP2], P66 [ROP1], and P68) in immunoglobulin G (IgG) and IgM recombinant enzyme-linked immunosorbent assays (Rec-ELISAs). Following an initial evaluation, six recombinant antigens (P29, P30, P35, P54, P66, and P68) were tested in the IgG and IgM Rec-ELISAs with four groups of samples which span the toxoplasmosis disease spectrum (negative, chronic infection, acute infection, and recent seroconversion). Our results suggest that the combination of P29, P30, and P35 in an IgG Rec-ELISA and the combination of P29, P35, and P66 in an IgM Rec-ELISA can replace the tachyzoite antigen in IgG and IgM serologic tests, respectively. The relative sensitivity, specificity, and agreement for the IgG P29-P30-P35 Rec-ELISA were 98.4, 95.7, and 97.2%, respectively. The resolved sensitivity, specificity, and agreement for the IgM P29-P35-P66 Rec-ELISA were 93.1, 95.0, and 94. 5%, respectively. Relative to the tachyzoite-based immunocapture IgM assay, the IgM P29-P35-P66 Rec-ELISA detects fewer samples that contain IgG antibodies with elevated avidity from individuals with an acute toxoplasmosis.
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PMID:Recombinant antigens to detect Toxoplasma gondii-specific immunoglobulin G and immunoglobulin M in human sera by enzyme immunoassay. 1069 10