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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nucleotide sequence analysis of the fae operon encoding the biosynthesis of K88 fimbriae revealed the presence of two divergently transcribed regulatory genes, faeA and faeB, separated by two inverted IS1 insertions. The amino acid sequences of the regulatory proteins FaeA and FaeB show similarity to the primary structure of corresponding regulatory proteins involved in the biosynthesis of Pap and S fimbriae. Expression of faeA is positively controlled by the FaeA protein, whereas K88 fimbriae production is negatively controlled by the co-operative activity of FaeA and the leucine-responsive regulatory protein (Lrp). Exchange of FaeA for Papl, a positive regulator of Pap fimbriae expression, also represses K88 production indicating that the combination Papl/Lrp has opposite effects on fae and pap expression. Mutations in faeB had no effect on the biosynthesis of K88 fimbriae. The presence of the two IS1 insertions is hypothesized to neutralize part of the repression of K88 biosynthesis by FaeA/Lrp. Like pap, the fae operon does not respond to exogenous leucine.
Mol Microbiol 1994 Feb
PMID:Leucine-responsive regulatory protein, IS1 insertions, and the negative regulator FaeA control the expression of the fae (K88) operon in Escherichia coli. 815 76

The expression of an increasing number of genes of both prokaryotic and eukaryotic origin has been shown to be regulated at the translational level by programmed (sequence-specific) ribosomal frameshifting. Among these are the bacterial insertion sequences IS1 and two members of the widely distributed IS3-family, IS150 and IS911. Frameshifting provides a means of specifying several proteins with different functions using a minimum of genetic information. In this review, we survey present understanding of the way in which frameshifting is integrated into the overall control of transposition activity in these elements.
Mol Microbiol 1993 Feb
PMID:Translational frameshifting in the control of transposition in bacteria. 838 87

Strains in the genus Shigella are nonmotile, but they retain some cryptic flagellar operons whether functional or defective (A.Tominaga, M. A.-H. Mahmoud, T. Mukaihara, and M. Enomoto, Mol. Microbiol. 12:277-285, 1994). To disclose the cause of motility loss in shigellae, the presence or defectiveness of the flhD and flhC genes, composing the master operon whose mutation causes inactivation of the entire flagellar regulon, was examined in the four Shigella subgroups. The flhD operon cloned from Shigella boydii and Shigella sonnei can activate, though insufficiently, the regulon in the Escherichia coli flhD or flhC mutant background. The clone from Shigella dysenteriae has a functional flhD gene and nonfunctional flhC gene, and its inactivation has been caused by the IS1 element inserted in its 5' end. The operon of Shigella flexneri is nonfunctional and has suffered an IS1-insertion mutation at the 5' end of the flhD gene. Comparison of restriction maps indicates that only the central 1.8-kb region, including part of the flhC gene and its adjacent mot operon, is conserved among the four Shigella subgroups as well as in E. coli, but in Salmonella typhimurium the whole map is quite different from the others. Motility loss in shigellae is not attributable to genetic damage in the master operon of a common ancestor, but it occurs separately in respective ancestors of the four subgroups, and in both S. dysenteriae and S.flexneri IS1 insertion in the master operon might be the primary cause of motility loss.
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PMID:Detection and characterization of the flagellar master operon in the four Shigella subgroups. 868 72

Insertion sequence IS1 specifies the InsA, delta InsA-B'-InsB and InsA-B'-InsB protein species. These three proteins have the identical alpha-helix-turn-alpha-helix motif that is likely to be responsible for DNA binding. In fact, InsA binds to the ends of IS1, and regulates gene expression and transposition of IS1. delta InsA-B'-InsB and/or InsA-B'-InsB has been thought to possess a transposase-like activity. Here, I examined the actions of these proteins in vivo on the promoter (pinsL) in the left end of IS1. InsA repressed pinsL-driven gene expression, both in cis and in trans. delta InsA-B'-InsB inhibited it efficiently only when pinsL was located near the construct where delta InsA-B'-InsB is expressed. Furthermore, it has been shown that the possible -10 sequence of pinsL is required for delta InsA-B'-InsB to act on, but the -35 sequence where InsA binds specifically, is not. InsA-B'-InsB appeared not to work on a nearby pinsL. The cis-action of delta InsA-B'-InsB is consistent with the previous observation that the IS1 transposase acts preferentially in cis. Interestingly, delta InsA-B'-InsB acted on a nearby P3 promoter in the IS1 insertion hotspot, and on another promoter outside the hotspot. delta InsA-B'-InsB may generally interact with the regions in or around promoters owing to their low DNA helix stability. Note that IS1 transposes preferentially into A + T-rich DNA segments, and that DNA is unwound from the -10 region of a promoter in transcription. The cis-preference of delta InsA-B'-InsB would result in an overall reduction of transposition of IS1 and its defective copy in a cell, allowing stable existence of the element in its bacterial host.
J Mol Biol 1997 Apr 04
PMID:Genetic analyses of the interactions of the IS1-encoded proteins with the left end of IS1 and its insertion hotspot. 912 37

EcoR124l, EcoDXXl and Ecoprrl are the known members of the type IC family of DNA restriction and modification systems. The first three are carried on large, conjugative plasmids, while Ecoprrl is chromosomally encoded. The enzymes are coded by three genes, hsdR, hsdM and hsdS. Analysis of the DNA sequences upstream and downstream of the type IC hsd loci shows that all are highly homologous to each other and also to sequences present in the bacteriophage P1 genome. The upstream sequences include functional phd and doc genes, which encode an addiction system that stabilizes the P1 prophage state, and extend to and beyond pac, the site at which phage DNA packaging begins. Downstream of the hsd loci, P1 DNA sequences begin at exactly the same place for all of the systems. For EcoDXXl and Ecoprrl the P1 homology extends for thousands of base pairs while for EcoR124l and IS1 insertion and an associated deletion have removed most of the P1-homologous sequences. The significance of these results for the evolution of DNA restriction and modification systems is discussed.
Mol Microbiol 1997 Feb
PMID:The type IC hsd loci of the enterobacteria are flanked by DNA with high homology to the phage P1 genome: implications for the evolution and spread of DNA restriction systems. 915 44

We have studied the spatial distribution of IS1 elements in the genomes of natural isolates comprising the ECOR reference collection of Escherichia coli. We find evidence for nonrandomness at three levels. Many pairs of IS1 elements are in much closer proximity (< 10 kb) than can be accounted for by chance. IS1 elements in close proximity were identified by long-range PCR amplification of the genomic sequence between them. Each amplified region was sequenced and its map location determined by database screening of DNA hybridization. Among the ECOR strains with at least two IS1 elements, 54% had one or more pairs of elements separated by < 10 kb. We propose that this type of clustering is a result of "local hopping," in which we assume that a significant proportion of tranposition events leads to the insertion of a daughter IS element in the vicinity of the parental element. A second level of nonrandomness is found in strains with a modest number of IS1 elements that are mapped through the use of inverse PCR to amplify flanking genomic sequences: in these strains, the insertion sites tend to be clustered over a smaller region of chromosome than would be expected by chance. A third level of nonrandomness is observed in the composite distribution of IS elements across strains: among 20 mapped IS1 elements, none were found in the region of 48-77 minutes, a significant gap. One region of the E. coli chromosome, at 98 min, had a cluster of IS1 elements in seven ECOR strains of diverse phylogenetic origin. We deduce from sequence analysis that this pattern of distribution is a result of initial insertion in the most recent common ancestor of these strains and therefore not a hot spot of insertion. Analysis using long-range PCR with primers for IS2 and IS3 also yielded pairs of elements in close proximity, suggesting that these elements may also occasionally transpose by local hopping.
Mol Biol Evol 1997 Jul
PMID:Nonrandom location of IS1 elements in the genomes of natural isolates of Escherichia coli. 921 45

In growing Escherichia coli K12 cells, the cryptic bgl operon is activated 98% of the time by insertions of IS1 or IS5 into the control region, designated bglR. The activated bgl operon permits utilization of the beta-glucoside sugar arbutin as a sole carbon and energy source. The bgl operon is also activated by late-occurring mutations during prolonged selection on arbutin. The late-occurring mutations that occurred during prolonged carbon starvation in the presence of arbutin were "adaptive mutations" because they were specific to the presence of arbutin, and they did not occur during prolonged starvation in the absence of arbutin. The spectrum of late-arising mutations differed from that of early-arising, growth-dependent mutations in that 20% of the late-arising mutants resulted from mutations at the hns locus. This provides the first direct evidence for adaptive mutagenesis mediated by the insertion of IS elements. Because no special genetic background is required to select Bgl+ mutants, this affords the opportunity to study IS-element-mediated adaptive mutagenesis in a variety of genetic backgrounds, including the backgrounds of natural isolates of E. coli.
Mol Biol Evol 1998 Jan
PMID:Activation of the bgl operon by adaptive mutation. 949 99

Calpain 3 is a nonlysosomal cysteine protease whose biological functions remain unknown. We previously demonstrated that this protease is altered in limb girdle muscular dystrophy type 2A patients. Preliminary observations suggested that its gene is subjected to alternative splicing. In this paper, we characterize transcriptional and posttranscriptional events leading to alterations involving the NS, IS1, and IS2 regions and/or the calcium binding domains of the mouse calpain 3 gene (capn3). These events can be divided into three groups: (i) splicing of exons that preserve the translation frame, (ii) inclusion of two distinct intronic sequences between exons 16 and 17 that disrupt the frame and would lead, if translated, to a truncated protein lacking domain IV, and (iii) use of an alternative first exon specific to lens tissue. In addition, expression of these isoforms seems to be regulated. Investigation of the proteolytic activities and titin binding abilities of the translation products of some of these isoforms clearly indicated that removal of these different protein segments affects differentially the biochemical properties examined. In particular, removal of exon 6 impaired the autolytic but not fodrinolytic activity and loss of exon 16 led to an increased titin binding and a loss of fodrinolytic activity. These results are likely to impact our understanding of the pathophysiology of calpainopathies and the development of therapeutic strategies.
Mol Cell Biol 1999 Jun
PMID:Expression and functional characteristics of calpain 3 isoforms generated through tissue-specific transcriptional and posttranscriptional events. 1033 Jan 45

The pathogenicity of Erwinia herbicola pv. gypsophilae (Ehg) and Erwinia herbicola pv. betae (Ehb) is dependent on a native plasmid (pPATH(Ehg) or pPATH(Ehb)) that harbors the hrp gene cluster, genes encoding type III effectors, phytohormones, biosynthetic genes, and several copies of IS1327. Sequence analysis of the hrp-flanking region in pPATH(Ehg) (cosmid pLA150) revealed a cluster of four additional IS elements designated as ISEhel, ISEhe2, ISEhe3, and ISEhe4. Two copies of another IS element (ISEhe5) were identified on the upstream region of the indole-3-acetic acid operon located on the same cosmid. Based on homology of amino acids and genetic organization, ISEhe1 belongs to the IS630 family, ISEhe2 to the IS5 family, ISEhe3 and ISEhe4 to different groups of the IS3 family, and ISEhe5 to the IS1 family. With the exception of ISEhe4, one to three copies of all the other IS elements were identified only in pathogenic strains of Erwinia herbicola pv. gypsophilae and Erwinia herbicola pv. betae whereas ISEhe4 was present in both pathogenic and nonpathogenic strains. An open reading frame that exhibited high identity (89% in amino acids) to AvrPphD of Pseudomonas syringae pv. phaseolicola was present within the cluster of IS elements. An insertional mutation in the AvrPphDEh, reduced gall size in gypsophila by approximately 85%. In addition, remnants of known genes from four different bacteria were detected on the same cosmid.
Mol Plant Microbe Interact 2002 Jul
PMID:The presence of diverse IS elements and an avrPphD homologue that acts as a virulence factor on the pathogenicity plasmid of Erwinia herbicola pv. gypsophilae. 1211 87

Scoliosis, a lateral deviation of the spine frequently associated with rotation, is not a specific disease but a deformity complicating many diseases. Curve progression is the major concern irrespective of the initiating cause. Idiopathic scoliosis is arguably postural in nature and in some subjects develops from intrauterine compression. Analysis of the pathogenesis leads to the conclusion that progression is due to an accelerated premature osteoarthrosis induced by insidious tissue fatigue of biomechanical origin. The chronic cumulative effect of repetitive tensile stresses applied asymmetrically to the postural deformity, manifested by loss of tensile strength and tissue cohesion, leads to fragility and eventual tissue disintegration of vertebrae, intervertebral discs, and laxity of ligaments. Early treatment, prevention, and avoidance of stresses that accentuate progression are of paramount import.
Exp Mol Pathol 2003 Feb
PMID:Pathogenesis of idiopathic scoliosis revisited. 1264 32


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