No abstract

DNA fragments with ams genes of Erwinia amylovora and cps genes of Erwinia stewartii were transferred to exopolysaccharide (EPS)-deficient mutants of the other species. The resulting EPSs were characterized by sensitivity to EPS-dependent bacteriophages, staining with amylovoran-specific fluorescein-isothiocyanate-labelled lectin and chemical techniques, such as determination of the sugar composition and methylation analysis in order to distinguish between amylovoran and stewartan. Degradation by the stewartan-dependent phage ø-K9 was used to detect stewartan production, and staining with a lectin from Abrus precatorius detected amylovoran capsules. The patterns of sugar linkages were determined by methylation analysis. Stewartan contained a significantly higher glucose to galactose ratio than amylovoran and produced a characteristic signal from 6-linked glucose residues. By these criteria, most E. stewartii cps mutants displayed exclusively amylovoran synthesis when complemented with the ams cluster, and E. amylovora ams mutants complemented with E. stewartii cps genes produced stewartan. The complementation to an EPS-positive phenotype may require most genes of the ams or the cps operon. An exception was an E. stewartii cpsK mutant that made predominantly stewartan when complemented with the ams cosmid. IR spectra showed that both amylovoran and stewartan were acylated when synthesized in E. amylovora, but not in E. stewartii. The amylovoran-producing E. stewartii merodiploids regained virulence to corn seedlings when mucoidy was restored by the ams cluster, but the stewartan-producing E. amylovora ams-lcps + strains were weakly virulent on pear slices and avirulent on apple seedlings.

No abstract

We examined 88 nonpapillary renal cell carcinomas for allelic loss at chromosome arm 14q and correlated the results to size, grade, and stage of these tumors. Fourteen highly polymorphic microsatellite markers on the long arm of chromosome 14 were used for deletion mapping. Loss of heterozygosity (LOH) at the smallest overlapping segment of 14q24.2-qter was seen in 42 of 88 tumors. There was no significant correlation between frequency of 14q LOH and size of tumors (P = 0.11). LOH was frequently seen in grade 2 and 3 tumors (55% and 73%, respectively) and in stage III and IV tumors (53% and 80%, respectively). We found a significant correlation between chromosome arm 14q LOH and nuclear grade (P < 0.001) and stage (P < 0.001) of tumors. These observations indicate the presence of a tumor-suppressor gene at chromosome segment 14q24.2-qter and demonstrate the usefulness of microsatellite analysis for assessing the possible clinical outcome of nonpapillary renal cell carcinomas.

Loss of heterozygosity (LOH) at chromosome 8p is associated with the progression of conventional (non‐papillary) renal cell carcinomas (RCC). To determine the tumor suppressor gene locus, we carried out a deletion mapping of chromosome 8p at 10 microsatellite loci in 96 RCCs. LOH occurred in 32% of the tumors. The smallest overlapping region of deletion at chromosome 8p11.2–p23.1 corresponds to approximately 34‐cM genetic distance. No small interstitial deletion was seen. Int. J. Cancer 80:22–24, 1999. © 1999 Wiley‐Liss, Inc.