We have isolated mutants of Escherichia coli which do not support stable maintenance of mini-F plasmids (Accd rep' sop'). These host mutations, named hop, were classified into five linkage groups on the E. coli chromosome. Genetic analyses of these hop mutations by Hfr mating and P1 transduction showed their loci on the E. coli genetic map to be as follows: hopA in the gyrB-tnaA region, hopB in the bglB-oriC region, hopD between 8 The F and mini-F plasmids of Escherichia coli are stably maintained during cell division, despite the low copy number per cell (for review, see references 14, 16, and 20). Mini-F plasmids, which were constructed in vitro from the 9.6-kilobase (kb) EcoRI-generated f5 fragment of the F plasmid, have a partition mechanism which guarantees the exact partitioning of plasmid DNA molecules into both daughter cells at cell division. The partitioning is controlled by the products of the plasmid genes sopA and sopB and the DNA sequence of the cis-acting sopC region of the plasmid (13,22,29). The DNA sequence of the entire region involving sopA, sopB, and sopC has been described (27). In the sopC region, 12 direct repeats of the 43-base-pair (bp) motif were found (13, 27). The product of the sopB gene binds specifically to the sopC region (12,21).In the present paper, we describe the isolation and characterization of host chromosomal mutants which do not support stable maintenance of mini-F plasmids.MATERIALS AND METHODS Bacterial strains, plasmids, and phages. Derivatives of E. coli K-12 used are shown in Table 1. Mini-F plasmids pXX325 and pXX326, which have the partition segment carrying the sopA, sopB, and sopC genes but not the ccd segment, were described previously (30). Mini-F plasmid pXX327, which lacks both the sop and ced segments, was also described previously (15,30). These mini-F plasmids carry the bla gene conferring ampicillin resistance. P1 plasmid X-P1:SR cI857 Dam Kmr was provided by Michael B.Yarmolinsky. This plasmid does not have the postsegregational killing mechanism of plasmid-free segregants. pUC13 (36), pSC101 (9, 10), pOU47 (11), and pKP1033 (25) were used. Phage X imm2" precA+ was obtained from Mutsuo Imai. Phage P1 vir was used for transduction.Media. L medium (1% Bacto Tryptone [Difco Laboratories], 0.5% yeast extract, 0.5% NaCl, pH 7.4) and P medium (1% polypeptone, 0.5% NaCl, pH 7.4), which were supple-* Corresponding author. mented with thymine (50 jig/ml), were used. In pyrimidinerequiring mutants, uracil (50 ,g/ml) was added to P medium. A synthetic minimal medium, medium E (37), supplemented with 0.5% glucose and appropriate chemical compounds, was used to test requirements of cells. To test expression of P-galactosidase, X-gal plates (P medium containing 40 ,ug of 5-bromo-4-chloro-3-indolyl-p-D-galactopyranoside [X-gal] per ml) were used. For agar plates, 1.4% (wt/vol) agar was added. Antibiotics were used at the following concentrations: ampicillin, 25 pug/ml; tetracycline, 15 ,ug/ml; streptomycin, 100 ,ug/ml; kanamycin, 20 ,ug/ml.Construction of plasmid ...
BackgroundFocal segmental glomerulosclerosis (FSGS) lesions have often been discussed as a negative predictor in idopathic membranous nephropathy (MN). The mechanism of the development of FSGS lesion in MN is still uncertain.MethodsFrom 250 cases of MN, 26 cases contained FSGS lesion. We compared the clinicopathological characteristics between MN cases with FSGS lesion [MN-FSGS(+)] and MN without FSGS lesion [MN-FSGS(−)], matched for gender, age, stage of MN.ResultsThe glomerular filtration rate (eGFR) was significantly lower in MN-FSGS(+) cases compared to MN-FSGS(−), although nephrotic syndrome, hematuria, and systolic blood pressure levels were not significantly different between the two groups. Pathologically, glomeruli in MN-FSGS(+) cases showed narrowing and loss of glomerular capillaries with separating from GBM or disappearance of CD34+ endothelial cells, and accumulation of extracellular matrix (ECM) in capillary walls, indicating the development of glomerular capillary injury. These findings of endothelial injury were seen even in MN-FSGS(−) cases, but they were more prominent in MN-FSGS(+) than MN-FSGS(−) by computer assessed morphometric analysis. In MN-FSGS(+) cases, 44 out of 534 glomeruli (8.2%) contained FSGS lesions (n = 31, NOS lesion; n = 13, perihilar lesion). Significant thickness of GBM with ECM accumulation was evident in MN-FSGS(+) cases. Podocyte injury with effacement of foot processes was also noted, but the expression of VEGF on podocytes was not different between the two groups, which suggests that the significant thickness of capillary walls may influence the function of VEGF from podocyte resulting in the glomerular capillary injury that contribute to the development of FSGS lesion in MN.ConclusionGlomerular capillary injury was seen in all MN cases. Furthermore, the prominent injuries of glomerular capillaries may be associated with the deterioration of eGFR and the formation of FSGS lesions in MN.
Fig. 1. A postcontrast CT showed a 10×10× 8.5 cm mass adjacent to the inferior lateral portion of the left kidney. The mass exhibited inhomogeneous minimal enhancement with slightly higher attenuation than the skeletal muscle. The left renal vein and the inferior vena cava were visualized clearly. 199Magnetic Resonance in Medical Sciences, Vol. 2, No. 4, p. 199-202, 2003 Malignantˆbrous histiocytoma (MFH) arising from the renal capsule is a rare tumor. We report a case of 55-year-old man with this tumor. Radiological imaging, including magnetic resonance (MR) imaging, was helpful in the diŠerential diagnosis between MFH of the renal capsule and other renal tumors. In particular, a hypointense area identiˆed on T 2 -weighted images re‰ecting theˆbrous component was identiˆed as an important characteristic of renal MFH.
hopA mutants, which have been suggested to be defective in mini-F plasmid partitioning (H. Niki, C. Ichinose, T. Ogura, H. Mori, M. Morita, M. Hasegawa, N. Kusukawa, and S. Hiraga, J. Bacteriol. 170:5272-5278, 1988), were found to carry mutations in the gyrB gene, coding for the B subunit of DNA gyrase. In gyrB(HopA) mutants, relaxation of the superhelicity of plasmids, increased IncG incompatibility, and increased SopB protein production were observed. It is suggested that altered expression of the sop genes, which is due to relaxation of the mini-F plasmid DNA, causes both defective partitioning of the mini-F plasmids and increased IncG incompatibility in gyrB(HopA) mutants.
Benign lymphoepithelial lesions of the salivary glands associated with Sjögren's syndrome are characterized by extensive infiltration of lymphoid cells, atrophy of acini and the presence of so-called epimyoepithelial islands. This report describes ultrastructural and three-dimensional reconstructive studies of epimyoepithelial islands performed at Tokyo Women's Medical College. Ultrastructural examination showed that these islands are composed mainly of epithelial cells containing intermediate filaments and/or tonofilament bundles, scattered lymphocytes and plasma cells. Myoepithelium-like cells containing myofilaments were sometimes found in the peripheral portion of the myoepithelial islands. Also, mitotic figures were rarely found in these islands. Three-dimensional reconstructive study revealed that the epimyoepithelial islands are not isolated cell clusters but are continuous hypertrophic duct-like structures. These results suggest that the epimyoepithelial islands are derived from proliferating duct epithelial cells, especially those of large peripheral ducts.
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