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)

A collection of about 2500 clones containing hybrid plasmids representative of nearly the entire genome of B. subtilis 168 was established in E. coli SK1592 by using the poly(dA).poly(dT) joining method with randomly sheared DNA fragments and plasmid pHV33, a bifunctional vector which can replicate in both E. coli and B. subtilis. Detection of cloned recombinant DNA molecules was based on the insertional inactivation of the Tc gene occurring at the unique BamHI cleavage site present in the vector plasmid. Thirty individual clones of the collection were shown to hybridize specifically with a B. subtilis rRNA probe. CCC-recombinant plasmids extracted from E. coli were pooled in lots of 100 and used to transform auxotrophic mutants of B. subtilis 168. Complementation of these auxotrophic mutations was observed for several markers such at thr, leuA, hisA, glyB and purB. In several cases, markers carried by the recombinant plasmids were lost from the plasmid and integrated into the chromosomal DNA. Loss of genetic markers from the hybrid plasmids did not occur when a rec- recipient strain of B. subtilis was used.
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PMID:Construction of a colony bank of E. coli containing hybrid plasmids representative of the Bacillus subtilis 168 genome. Expression of functions harbored by the recombinant plasmids in B. subtilis. 11 26

Several conditional-lethal mutantions that do not permit the replication of F-factors of Escherichia coli K-12 are located at a site called seg. This gene is located on the E. coli chromosome between ser B and thr. It is unrelated to other known genes involved in DNA replication. Strains carrying seg mutations were unable to replicate F'-lac+, several F'-gal+s, F'-his+ and bacteriophage gamma at 42 degrees. However, neither phage T4, ColE1, nor any of the R factors tested were prevented from replicating at 42 degrees C. When the kinetics of the loss of F-primes is studied in seg strains, it is found that the rate of curing depends on the size of the plasmid, larger F factors curing faster than smaller ones, and that Hfrs are formed at high frequencies. The Hfrs showed both F-genote enlargement and normal transfer of chromosomal markers. The F-genotes are unstable and segregate chromosomal markers at high frequencies. Some orthodox Hfrs were examined, and two that were known to revert to the F+ condition relatively frequently were found to generate enlarged F-genotes on mating, whereas two strains that were very stable with respect to the F+ state did not show F-genote formation. F-genote formation from seg Hfr stains is dependent on a functional recA gene, as F-genote formation was not seen with a seg-2, recA-1 Hfr. This is in contrast to F-genote enlargement shown by both orthodox Hfrs and an Hfr strain constructed by integration of a temperature-sensitive F'-gal+, whose F-genote enlargement is Rec-independent. Thus there may be more than one mechanism for the formation of enlarged F-genotes.
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PMID:Plasmid replication and Hfr formation in strains of Escherichia coli carrying seg mutations. 32 Apr 53

For insertional mutagenesis of Pseudomonas aeruginosa, a derivative of the kanamycin-resistance (KmR) transposon Tn5 was constructed (Tn5-751) that carried the trimethoprim-resistance (TpR) determinant from plasmid R751 as an additional marker. Double selection for KmR and TpR avoided the isolation of spontaneous aminoglycoside-resistant mutants which occur at high frequencies in P. aeruginosa. As a delivery system for the recombinant transposon, plasmid pME305, a derivative of the broad-host-range plasma RP1, proved effective; pME305 is temperature-sensitive at 43 degrees C for maintenance in Escherichia coli and P. aeruginosa and deleted for IS21 and the KmR and primase genes. In matings with an E. coli donor carrying pME9(= pME305::Tn5-751), transposon insertion mutants of P. aeruginosa PAO were recovered at approx. 5 X 10(-7)/donor at 43 degrees C. Among Tn5-751 insertional mutants 0.9% were auxotrophs. A thr::Tn5-751 mutation near the recA-like locus rec-102 is useful for the construction of recombination-deficient strains. Several arc::Tn5-751 mutants could be isolated that were defective in anaerobic utilization of arginine as an energy source. From three of these mutants the arc gene region was cloned into an E. coli vector plasmid. Since Tn5-751 has a single EcoRI site between the TpR and KmR genes, EcoRI-generated fragments carrying either resistance determinant plus adjacent chromosomal DNA could be selected separately in E. coli. Thus, a restriction map of the arc region was constructed and verified by hybridization experiments. The arc genes were tightly clustered, confirming earlier genetic evidence.
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PMID:Transposon insertion mutagenesis of Pseudomonas aeruginosa with a Tn5 derivative: application to physical mapping of the arc gene cluster. 298 92

The frequency of genetic exchanges between F' factors and the bacterial chromosome was studied in recombination-deficient Escherichia coli mutants under conditions in which the recombinant F' factors were immediately transferred to new hosts. In a series of double matings, F101-1 thr(+)leu(-) episomes were first transferred into each of four intermediate F(-)thr(-)leu(+) strains carrying various rec alleles. After the original F' donors were killed with phage T6, the F101-1 episomes were then transferred from the intermediate cells to F(-)thr(-)leu(-)Str(R)recA(-) females. Recipients of nonrecombinant episomes formed Thr(+) (Str(R)) colonies, and recipients of recombinant episomes formed Leu(+)(Str(R)) colonies. A comparison of the numbers of Leu(+)(Str(R)) and Thr(+)(Str(R)) colonies shows that recB(-) males formed 18 to 21% and recC(-) formed 47 to 60% of the wild-type level of recombinant episomes that could be detected after transfer. No recombinant episomes were detected using a recA(-) intermediate strain. If the intermediate strains harboring the F101 episomes were purified, allowed to grow for 50 generations, and then mated with the recA(-) recipient, recombinant episomes were transferred at 8% of the wild-type level for recB(-) and 13% for recC(-). In contrast, only 0.4 and 0.6% of the normal number of recombinants were obtained from crosses between Hfr Cavalli donors and the same recB(-) and recC(-) strains. Recombinant episomes were detected with greater frequency among newly formed rec(+), recB(-), and recC(-) partial diploids than in those which were 50 generations old.
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PMID:Recombinant F' factors from Escherichia coli K-12 strains carrying recB or recC. 455 37

Mutants (phenotypic symbol Ref-II) refractory to colicin E2 have been isolated in several strains of Escherichia coli K-12, and a refII locus has been mapped 1 to 2 min counter clockwise to thr. A small number of Ref-II mutants are also ultraviolet (UV)-sensitive and the uv(s) locus in one such strain has been mapped close to the refII locus near thr. The Ref-II mutation alone does not affect recombinant formation in F(-) strains, but the Ref-II, UV(s) strains behave in many respects like Rec(-) mutants, giving reduced recombination frequencies in crosses with male strains. It is suggested that the refII and uv(s) loci correspond to closely linked if not identical genes, concerned in some way in the activity of one or more deoxyribonucleases, and that the Ref-II, UV(s) mutants arise as the pleiotropic expression of a single gene or of a deletion or polar mutation affecting linked genes.
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PMID:Identification of closely linked loci controlling ultraviolet sensitivity and refractivity to colicin E2 in Escherichia coli. 488 26

The rec-102 mutation had pleiotropic effects in Pseudomonas aeruginosa: low recombinational proficiency in conjugation and transduction; high UV sensitivity; inability to induce pyocin R2 by mitomycin C; and increased susceptibility to mitomycin C and nalidixic acid. The rec-102 locus was mapped by R68.45-mediated conjugation in the 45 min region of the PAO chromosome, between argF and thr-9001. By selection for a marker in this region, rec-102 can be introduced into a P. aeruginosa strain of interest using an R68.45 rec-102 donor. The recombination-deficient strains constructed in this way were phenotypically similar to Escherichia coli recA mutants.
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PMID:Construction of recombination-deficient strains of Pseudomonas aeruginosa. 641 24

Syndecan-4 (syn-4), a transmembrane heparan sulfate-containing proteoglycan, is unique among the four members of the syndecan family in its specific cellular localization to complex cytoskeletal adhesion sites, i.e., focal adhesions. During early phenotypic redifferentiation of neonatal cardiomyocytes in culture, immunolocalization reveals syn-4 to be heavily concentrated in the perinuclear endoplasmic reticulum-Golgi region, with little found at the peripheral regions. Subsequently, syn-4 becomes localized to a cytoskeletal adhesion complex unique to striated muscle, the costamere. Soon after redifferentiation of myofibrils in cultured neonatal cardiomyocytes, syn-4 is present only in costameres, not in focal adhesions. In cultured adult cardiomyocytes, it is present in both costameres and focal adhesions-the latter in two distinct regions of the spread cardiomyocytes, reflecting localization with two types of actin-containing filaments. The fact that syn-4 is observed early in the costameric regions, as opposed to later in the focal adhesions, suggests that it may play an initial role in early adhesion/signal transduction mechanisms in close proximity to the contractile apparatus, as well as in transmission of contractile force to the collagenous extracellular matrix (ECM) which surrounds the cardiac myofibers in situ. With respect to possible regulatory mechanisms of syn-4, we localized syn-4 with both the epsilon isoform of protein kinase C and the tyrosine kinase pp60(csrc) in costameric regions. These findings suggest that syn-4 may not only play a role in cellular adhesion and contractile force transmission, it may also, through ser, thr, and tyr phosphorylation, be part of an interactive signal transduction mechanism in myocardial functioning via these adhesive cytoskeletal complexes.
Anat Rec 2002 Sep 01
PMID:Localization of the transmembrane proteoglycan syndecan-4 and its regulatory kinases in costameres of rat cardiomyocytes: a deconvolution microscopic study. 1220 63