Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P06889 (Mol)
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Our isolate of Tn7 (named Tn7S ) contains an IS1 insertion, and this IS1 can be converted into Tn9. In vitro and in vivo deletions of Tn7S and Tn7S ::Tn9 define regions of the transposon required for antibiotic resistance and transposition. Complementation of deletion mutants by cloned Tn7 fragments indicates the existence of two regions, denoted tnp7A and tnp7B , required for all transposition events. Another region, denoted tnp7C , is required for transposition from the chromosome to RP1 but not for transposition from a small IncP-1 replicon to the chromosome. The presence of Tn7S terminal sequences in an RP1 replicon reduces the transposition of a second Tn7S derivative from the chromosome by about one order of magnitude. The measured frequency of Tn7S transpositions from a small IncP-1 replicon to the chromosome depends on the particular incompatibility system used to eliminate that replicon. Genetic and physical data indicate that high frequencies of Tn7S transposition to the chromosome (greater than or equal to 40%) are triggered by the IncP-1 incompatibility reaction, thus suggesting the existence of a Tn7 mechanism for sensing the state of the carrier replicon.
Mol Gen Genet 1984
PMID:Control of Tn7 transposition. 632 11

A plasmid pKY159 (Yamaguchi and Yamaguchi 1983) carrying a promoter proximal portion of the gene cluster of the proton-translocating ATPase (H+-ATPase) of Escherichia coli causes growth inhibition of wild-type cells. Insertion of a transposable element in this plasmid released this inhibitory effect. In analyzing this inhibitory effect, we determined the insertion points at the nucleotide-sequence level of transposable elements on 30 independent derivatives of pKY159 . Insertions of IS1, IS5, and gamma delta were found between the promoter and the gene for a possible component of 14,000 daltons of the H+-ATPase. Of 31 insertions, 26 were of IS1 and were located at the same site, indicating that this site is a hotspot for IS1 insertion and that IS1 insertion is much more frequent than that of IS5 or gamma delta in this region. Four different sites for IS1 insertion were found; in two of these an 8 base pair (bp) duplicate of the target sequence ( AAAAACGT and AAACGTTG ) was generated, while in the other two a 9 bp duplicate was found. In all cases in this study the nucleotide sequence of IS1 was the same as that of IS1-K. In the two cases with an 8 bp duplicate in different sites, a common 6 bp sequence ( AAACGT ) was found. These results suggested that generation of the 8 bp duplicate is related to the common sequence rather than a mutation in IS1 suggested by Iida et al. (1981) and also suggested that the essential length of the duplicate is 8 bp or less than 8 bp. A 6 bp sequence ( GTGATG ) homologous to the end portion of IS1 was found at the hotspot , but not at other sites, suggesting that this homology contributed to the high frequency of IS1 insertion.(ABSTRACT TRUNCATED AT 250 WORDS)
Mol Gen Genet 1984
PMID:Insertions of transposable elements in the promoter proximal region of the gene cluster for Escherichia coli H+-ATPase: 8 base pair repeat generated by insertion of IS1. 632 13

Plasmid Rms312, specifying resistance to tetracycline (Tc), chloramphenicol (Cm), streptomycin (Sm), sulfonamide (Su), and mercury chloride (Mer), deletes both Tc and Cm Sm Su Mer determinants at a high frequency in Salmonella typhimurium LT2. S. typhimurium mutants that were stable carriers of Rms312 were isolated by alternate culture of R-bearing cells in a medium containing either tetracycline or chloramphenicol. In one of these mutants the deletion frequency of drug resistance determinants was decreased by about 100-fold not only Rms312, but also in R100, R1, and R6-5. This mutation caused a slight reduction of ultraviolet resistance but did not affect generalized genetic recombination, indicating that the mutation is different from recA. The mutation, designated dor (deletion of r-determinants), was mapped to a position near 57 units in the new linkage map of S. typhimurijm LT2 (K. E. Sanderson and P. E. Hartman, Microbiol. Rev. 42:471-519, 1978). The dor mutation had no effect on IS1-mediated illegitimate deletion, indicating that the dor mutation is different from the del mutation described by Nevers and Saedler (P. Nevers and H. Saedler, Mol. Gen. Genet. 160:209-214, 1978).
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PMID:Salmonella typhimurium LT2 mutation affecting the deletion of resistance determinants on R plasmids. 698

The replication of a spontaneous Kil- mutant of bacteriophage Mu has been investigated. The Kil- mutation (Mucts62-13/4), which was introduced into a defective prophage, is pleiotrophic, leading to the loss of also the Gam, Cim and Sot functions. The mutation is caused by an insertion with the characteristics of IS1, located just outside the B gene. Mucts62-1 3/4 phages form extremely small plaques on wildtype indicator strains. The replication of the insertion mutant as compared to Mucts62 is strongly reduced. Normal replication could be restored by relieving the polarity of the insertion or by complementation with defective prophages which express all early functions. Apparently, early genes other than A and B are involved in normal Mu DNA replication.
Mol Gen Genet 1982
PMID:Bacteriophage Mu DNA replication is stimulated by non-essential early functions. 705 Jun 22

Expression of the K88 (fae) operon is negatively controlled by the co-operative binding of Lrp and FaeA to the fae regulatory region and is dependent on the methylation status of three GATC sites present in this region. In this paper, we describe the binding of Lrp to a T-rich DNA helix between GATC site I and site II. FaeA stabilized and modified the Lrp binding, thereby extending the Lrp footprint over GATC site I and site III. Methylation of GATC site I prevented the binding of Lrp/FaeA at this site and appeared to be essential for the cells, since mutation of this site into GTTC resulted in a lethal overproduction of K88 fimbriae. Methylation of GATC site II and site III reduced the stability of Lrp/FaeA binding. Moreover, methylation of GATC site III stimulated faeB promoter activity. The plasmid population in cells harbouring multiple copies of a K88 plasmid consisted of two differentially methylated forms. Form A plasmids with a methylated GATC site I and site III and a nonmethylated site II (+,-,+) represented 20% of the population and were responsible for high-level expression. Form B plasmids with a methylated GATC site I and a non-methylated site II and site III (+,-,-) represented 80% of the population and were responsible for low-level expression. Apparently, K88 fimbriae expression in vivo is balanced at its maximal possible level by modulation of the methylation status of GATC site III. The ratio (1:4) between these populations is stabilized by a constitutive synthesis of FaeA resulting from the presence of an IS1 insertion upstream of faeA. This IS1 insertion separates the faeA promoter from the FaeB-binding sites, thereby neutralizing the control by FaeB activity on expression of FaeA. Instead, faeA transcription is stimulated by binding of FaeA to the faeA promoter region.
Mol Microbiol 1995 Jun
PMID:Negative control of fae (K88) expression by the 'global' regulator Lrp is modulated by the 'local' regulator FaeA and affected by DNA methylation. 747 91

The mechanism of folding of the small protein barstar in the pre-transition zone at pH 7, 25 degrees C has been characterized using rapid-mixing techniques. Earlier studies had established the validity of the three-state US <--> UF <--> N mechanism for folding and unfolding in the presence of guanidine hydrochloride (GdnHCl) at concentrations greater than 2.0 M, where US and UF are the slow-refolding and fast-refolding unfolded forms, respectively, and N is the fully folded form. It is now shown that early intermediates, IS1 and IS2 as well as a late native-like intermediate, IN, are present on the folding pathways of US, and an early intermediate IF1 on the folding pathway of UF, when barstar is refolded in concentrations of GdnHCl below 2.0 M. The rates of formation and disappearance of IN, and the rates of formation of N at three different concentrations of GdnHCl in the pre-transition zone have been measured. The data indicate that in 1.5 M GdnHCl, IN is not fully populated on the US-->IS1-->IN-->N pathway because the rate of its formation is so slow that the US <--> UF <--> N pathway can effectively compete with that pathway. In 1.0 M GdnHCl, the US-->IS1-->IN transition is so fast that IN is fully populated. In 0.6 M GdnHCl, IN appears not to be fully populated because an alternative folding pathway, US-->IS2-->N, becomes available for the folding of US, in addition to the US-->IS1-->IN-->N pathway. Measurement of the binding of the hydrophobic dye 1-anilino-8-naphthalenesulphonate (ANS) during folding indicates that ANS binds to two distinct intermediates, IM1 and IM2, that form within 2 ms on the US-->IM1-->IS1-->IN-->N and US-->IM2-->IS2-->N pathways. There is no evidence for the accumulation of intermediates that can bind ANS on the folding pathway of UF.
J Mol Biol 1995 Apr 14
PMID:The folding mechanism of barstar: evidence for multiple pathways and multiple intermediates. 772 34

Incomplete splicing is essential for retroviral replication; and in simple retroviruses, splicing regulation appears to occur entirely in cis. Our previous studies, using avian sarcoma virus, indicated that weak splicing signals allow transcripts to escape the splicing pathway. We also isolated a series of avian sarcoma virus mutants in which env mRNA splicing was regulated by mechanisms distinct from those of the wild-type virus. In vitro splicing experiments with one such mutant (insertion suppressor 1 [IS1]) revealed that exon 1 and lariat-exon 2 intermediates were produced (step 1) but the exons were not efficiently ligated (step 2). In this work, we have studied the mechanism of this second-step block as well as its biological relevance. Our results show that the second-step block can be overcome by extending the polypyrimidine tract, and this causes an oversplicing defect in vivo. The requirement for regulated splicing was exploited to isolate new suppressor mutations that restored viral growth by down-regulating splicing. One suppressor consisted of a single U-to-C transition in the polypyrimidine tract; a second included this same change as well as an additional U-to-C transition within a uridine stretch in the polypyrimidine tract. These suppressor mutations affected primarily the second step of splicing in vitro. These results support a specific role for the polypyrimidine tract in the second step of splicing and confirm that, in a biological system, uridines and cytosines are not functionally equivalent within the polypyrimidine tract. Unlike the wild-type virus, the second-step mutants displayed significant levels of lariat-exon 2 in vivo, suggesting a role for splicing intermediates in regulation. Our results indicate that splicing regulation can involve wither the first or second step.
Mol Cell Biol 1995 May
PMID:Genetic selection for balanced retroviral splicing: novel regulation involving the second step can be mediated by transitions in the polypyrimidine tract. 773 46

We find that IS1 transposase, like that of Tn10, can induce the SOS response when produced at high levels. Most of the activity (> 80%) requires IS1 ends in cis to the transposase gene and depends strictly on the presence of RecBCD function. This implies that processing of transposase-induced cleavages is responsible for generating the response. Induction of the SOS response during growth in a rich medium is seen only when cells approach stationary phase. The end-dependent induction is abolished by mutations in the ends of IS1 that eliminate transposition activity. IS1 ends in identical orientation on the same plasmid are inactive in transposition but stimulate SOS strongly. Even plasmids with a single end can stimulate SOS, probably as a consequence of plasmid dimer formation which places the ends in direct repeat orientation. These results imply that transposase-induced cleavages do not need inversely oriented ends. The system can therefore be used to dissociate cleavage activity from the other reactions of transposition. Induction of SOS by a series of short (67 to 114 bp) IS1-like elements was found to occur in a cyclical pattern as a function of length with a period of 10 to 11 bp. The frequency of cointegration promoted by these elements showed the same helix-phase dependence. These results suggest that transposase molecules bound to the ends of IS1 interact, and that this interaction is needed for the cleavages that initiate transposition.
J Mol Biol 1994 Sep 30
PMID:Induction of the SOS response by IS1 transposase. 793 94

Insertion sequence IS1 contains two reading frames, insA and B'-insB, which are responsible for its transposition, and was previously shown to express two proteins. The first, InsA, is the product of insA. The second, InsA-B'-InsB is a fusion of InsA with the product of B'-insB. Synthesis of this protein occurs by a -1 frameshift from the 3' region of the insA frame to the open reading frame B', extending from the 5' end of the insB frame. Here, I have shown genetically that IS1 encodes the third species delta InsA-B'-InsB: delta InsA-B'-InsB uses two alternative initiation codons in the middle of the insA frame, and is produced by a frameshift mechanism similar to that used in InsA-B'-InsB expression. Deletion of the small region preceding these initiation codons resulted in decreased expression of delta InsA-B'-InsB, suggesting that the small region play some role in the translation initiation. Surprisingly, it was found that delta InsA-B'-InsB has a transposase-like function and InsA can stimulate the transposition promoted by delta InsA-B'-InsB, while delta InsA-B'-InsB seemed to bind to the left terminal inverted repeat (IRL) of IS1 and inhibit transposition when it was present in excess, as well as InsA represses transposition. It is likely that IS1 transposition activity depends on the ratio of InsA to delta InsA-B'-InsB. A double missense mutation of the internal initiation codons resulted in decreased cointegration activity, showing that delta InsA-B'-InsB is responsible for transposition but InsA-B'-InsB is probably not. Some IS elements, which also contain two tandem, out-of-phase, overlapping genes, appear to express deleted fusion proteins like delta InsA-B'-InsB, but the functions are unknown. The complex phenomena of transposition and its control found in IS1 may be more general in the other mobile DNAs.
J Mol Biol 1994 Jul 01
PMID:Genetic evidence for IS1 transposition regulated by InsA and the delta InsA-B'-InsB species, which is generated by translation from two alternative internal initiation sites and frameshifting. 802 40

Sequence determination of the chloroplast clpP gene from two distantly related Chlamydomonas species (C. reinhardtii and C. eugametos) revealed the presence of translated large insertion sequences (IS1 and IS2) that divide the clpP gene into two or three sequence domains (SDs) and are not found in homologous genes in other organisms. These insertion sequences do not resemble RNA introns, and are not spliced out at the mRNA level. Instead, each insertion sequence forms a continuous open reading frame with its upstream and downstream sequence domains. IS1 specifies a potential polypeptide sequence of 286 and 318 amino acid residues in C. reinhardtii and C. eugametos, respectively. IS2 encodes a 456 amino acid polypeptide and is present only in C. eugametos. The two Chlamydomonas IS1 sequences show substantial similarity; however, there is no significant sequence similarity either between IS1 and IS2 or between these insertion sequences and any other known protein coding sequences. The C. reinhardtii clpP gene was further shown to be essential for cell growth, as demonstrated through targeted gene disruption by particle gun-mediated chloroplast transformation. Only heteroplasmic transformants could be obtained, even under mixotrophic growth conditions. The heteroplasmic transformants were stable only under selection pressure for the disrupted clpP, rapidly segregated into wild-type cells when the selection pressure was removed, and grew significantly more slowly than wild-type cells under phototrophic conditions.
Mol Gen Genet 1994 Jul 25
PMID:The Chlamydomonas chloroplast clpP gene contains translated large insertion sequences and is essential for cell growth. 805 34


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