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Query: UNIPROT:P06889 (Mol)
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Infection of Mu-sensitive bacteria with a recombinant lambda phage that carries the EcoRI.C fragment from the immunity end of wild type Mu DNA causes filamentous growth. Transmission electron microscopy revealed that the cell-division cycle was inhibited at, or prior to, the initiation of septation. The filamentation does not occur after infection of Mu-immune bacteria or after infection with a phage carrying the same EcoRI.C fragment, but with an IS1 insertion in gene B of Mu, showing that either gpB and/or some non-essential functions (e.g. kil) mapping downstream from the insertion are required for the inhibition of cell division. These data and previously published evidence suggest that in the "killing" of E. coli K12 by early Mu functions expressed from the cloned EcoRI.C fragment, two components have to be distinguished: one, a highly efficient elimination of plasmid DNA carrying the early Mu genes, and second, a series of interactions with host functions conducent to an inhibition of cell division. It is suggested that functions normally involved in the SOS reaction participate in the inhibition of cell division by early Mu functions. Infected bacteria synthesize the replication protein B (MR 33000) of Mu, which was found by cell fractionation experiments to be associated with the inner cell membrane. The role of this association for filamentous growth and for the integrative replication of the phage is discussed. The recombinant phage might be useful as a tool for the study of the E. coli cell division cycle.
Mol Gen Genet 1986 Mar
PMID:Inhibition of bacterial segregation by early functions of phage mu and association of replication protein B with the inner cell membrane. 352 Feb 39

The nucleotide sequence analysis of insertion element IS1 has shown that IS1 could have as many as six translational reading frames encoding possible proteins. In order to determine which reading frames are actual structural genes responsible for IS1-mediated recombination, we introduced base substitution mutations including nonsense mutations into all of the potential reading frames and examined the ability of these IS1 mutants to mediate cointegration between two plasmids. The results reveal that IS1 has two structural genes (termed insA and insB), which are required for plasmid cointegration mediated by IS1.
J Mol Biol 1984 Aug 05
PMID:Insertion element IS1 encodes two structural genes required for its transposition. 608 42

Escherichia coli RNA polymerase was found to bind specifically to restriction fragments containing either end of IS1. DNase I footprint analyses indicate that RNA polymerase protects approximately 70 base-pairs at each end of IS1, including the left or right terminal inverted repeat sequences in IS1 (termed insL or insR, respectively) as well as some non-IS1 sequence directly adjacent to each end of IS1. Analysis of transcripts from the left terminal region of IS1 shows that the insL sequence contains a promoter (named insPL), and that RNA synthesis initiates apparently at one in a stretch of five adenylate residues within insL and continues toward the interior region of IS1. Interestingly, most of the resulting transcripts contain polyuridylate residues (more than 5 U residues) at their 5'-ends. Analysis of transcripts from the right terminal region of IS1 indicates that the insR sequence also contains a promoter (named insPR). RNA synthesis initiates specifically at an adenylate residue within insR and continues toward the interior region of IS1, i.e. in the opposite direction to RNA synthesis initiating at insPL, which is present at the other end of IS1. We propose that insPL is used to make the messenger RNA for the IS1-encoded genes insA and insB, while insPR might be used to synthesize an anti-mRNA and thereby negatively regulate insPL.
J Mol Biol 1984 Aug 05
PMID:Both inverted repeat sequences located at the ends of IS1 provide promoter functions. 608 43

The nucleotide sequence of the rpsE gene for the ribosomal protein S5 of a mutant of E. coli showing cold-sensitive growth revealed the presence of an insertion sequence, IS1, near the 3'-end of the gene. This mutant grows very slowly even at the "permissive temperature" (30 degrees C). At temperatures below 20 degrees C, its growth becomes negligible. It is likely that the presence of IS1 disturbs the continued translation of the polycistronic messenger RNA of the "spc-operon" from the point of IS1 insertion downwards, especially at the unfavorable temperatures.
Mol Gen Genet 1984
PMID:Insertion of IS1 into the rpsE gene for ribosomal protein S5 causes cold-sensitivity in Escherichia coli. 609 60

The Escherichia coli mutant rho-115 suppresses lac operon polarity conferred by the lacZ::IS1 insertion MS319. The ATPase activity of purified rho-115 protein was maximal at 40 degrees C, in contrast to 45 degrees C for rho+. At higher temperatures (50 degrees C, 55 degrees C), the fractions of activities at maximal temperature were consistently lower for rho-115 compared to rho+. The 30-minute time course of rho-115 ATP hydrolysis was linear at 37 degrees C but at 45 degrees C the linear kinetics of hydrolysis reached a plateau between 10 and 15 minutes. The 30-minute time courses for rho+ were linear at both 37 degrees C and 45 degrees C. The rho-115 and rho+ ATPase activities were equally heat-stable during preincubation at 45 degrees C in buffer. Inclusion of ATP during preincubation protected these rho proteins from inactivation to the same extent. The presence of polyC during preincubation protected rho+ activity but produced substantial inactivation of rho-115 ATPase. The presence of polyU during preincubation gave similar results. Concentrations of polyC between 625 ng/ml and 100 micrograms/ml yielded the same extent of rho-115 ATPase inactivation during preincubation at 45 degrees C. Thermal inactivation of rho-115 ATPase by polyC was halted by shifting preincubation temperature from 45 degrees C to 35 degrees C, indicating that polyC-induced destabilization of rho-115 was irreversible.
Mol Gen Genet 1981
PMID:A mutant rho ATPase from Escherichia coli that is temperature-sensitive in the presence of RNA. 616 79

Inverse transposition of the DNA of pBR322 was found to be mediated by the small transposon Tn981 a relative of Tn9 flanked by direct repeats of IS1. Since the resulting structure IS1::pBR322::IS1 (Tn983) is transposed in a second step in the absence of Tn981, it is concluded that all the functions necessary for transposition of IS1 flanked transposons are coded for by IS1 itself or the E. coli chromosome, respectively.
Mol Gen Genet 1980
PMID:Genetic evidence for absence of transposition functions from the internal part of Tn981 a relative of Tn9. 624 12

Tn9 is a transposable element in which a gene (cat) determining chloramphenicol resistance is flanked by directly repeated sequences that are homologous to the insertion sequence IS1. We show here that infection of Escherichia coli K12 (under Rec-Red-Int- conditions) with a lambda bio transducing phage carrying Tn9 results in the formation of lambda bio transductants as frequently as cat transductants as frequently as cat transductants (about 1 per 10(6) to 10(7) infected cells). Most of the lambda bio transductants do not carry cat, just as most of the cat transductants do not carry lambda bio. In spite of the absence of cat, the lambda bio prophage can transpose a second time, from the E. coli chromosome to different sites on an F'gal plasmid. Analysis of the structure of the transposed lambda bio element, by restriction nuclease digestion and by electron microscopy, demonstrates that the integrated lambda bio prophage is flanked by directly repeated IS1 elements. We conclude that there is no genetic information for the ability to transpose encoded in the non-repeated portion of Tn9, i.e. that the directly repeated IS1 elements alone are responsible for Tn9 transposition.
Mol Gen Genet 1980 Apr
PMID:Transposition of IS1-lambdaBIO-IS1 from a bacteriophage lambda derivative carrying the IS1-cat-IS1 transposon (Tn9). 624 15

DNA-DNA filter binding tests, "Southern" blotting experiments and DNA heteroduplex analysis clearly show that Tn951 contains an IS1 element. This IS1-951 sequence is peculiar in that it does not contain the PstI cleavage site which is usually observed on E. coli derived IS1 elements. Nonetheless, IS1-951 induces deletions. This process is temperature dependent. One instance of an IS1-951 induced inversion was observed, the structure of which is compatible with the current models of transposition of IS elements.
Mol Gen Genet 1980
PMID:Deletions and an inversion induced by a resident IS1 of the lactose transposon Tn951. 624 27

IS1-mediated insertion and deletion formation occur preferentially into A+T-rich regions of DNA of bacteriophate P1 and of the r-determinant of the R plasmid NR1. The significance of this correlation is discussed in view of other published data.
Mol Gen Genet 1980
PMID:Does the insertion element IS1 transpose preferentially into A+T-rich DNA segments? 624 30

We describe ColEl-type plasmids, with relaxed DNA replication, based on pMB9, and carrying the CmR determinant of R1, in addition to the TcR determinant of pMB9. One of the plasmids, pPH207, has unique sites for EcoRI, HindIII, BamI, SalI and HpaI. Insertion of foreign DNA into all but the last of these inactivates either the CmR or the TcR determinant. The original CmR TcR plasmid (pCM2) contains a copy of IS1 which produces deletions to left and to right. Most of these inactivate either the CmR or the TcR determinant. An internal 280 bp deletion of IS1 DNA in pPH207 greatly reduces the frequency at which deletions are observed. The main feature of these plasmids is a site that is cleaved by some preparations of EcoRI in only one strand of the DNA duplex (the EcoRIn site). This site facilitates strand separation of sequences inserted at the HindIII, BamI and SalI sites of the TcR gene, and also of any inserted at the true EcoRI site by a method that destroys that site. Since the orientation of the EcoRIn site is known, the orientation of sequences inserted at the neighbouring sites can be easily determined. Plasmid pPH207 is not mobilised by a Hfr, but its mobilisation is promoted by ColEl. It is therefore Mob- bom+. Experiments with minicells show that it directs the copious synthesis of chloramphenicol transacetylase.
Mol Gen Genet 1980
PMID:Plasmid cloning vectors that can be nicked at a unique site. 625 86


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