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Importance of Hydrogen Sulfide, Thiosulfate, and Methylmercaptan for Growth of Thiobacilli during Simulation of Concrete Corrosion 总被引:4,自引:3,他引:1 下载免费PDF全文
Wolfgang Sand 《Applied microbiology》1987,53(7):1645-1648
Biogenic sulfuric acid corrosion of concrete surfaces caused by thiobacilli was reproduced in simulation experiments. At 9 months after inoculation with thiobacilli, concrete blocks were severely corroded. The sulfur compounds hydrogen sulfide, thiosulfate, and methylmercaptan were tested for their corrosive action. With hydrogen sulfide, severe corrosion was noted. The flora was dominated by Thiobacillus thiooxidans. Thiosulfate led to medium corrosion and a dominance of Thiobacillus neapolitanus and Thiobacillus intermedius. Methylmercaptan resulted in negligible corrosion. A flora of heterotrophs and fungi grew on the blocks. This result implies that methylmercaptan cannot be degraded by thiobacilli. 相似文献
23.
Transposon Mutants of Bradyrhizobium japonicum Altered in Attachment to Host Roots 总被引:1,自引:0,他引:1 下载免费PDF全文
Transposon mutants of Bradyrhizobium japonicum 110 ARS were produced and screened for changes in attachment ability. Mutant CFK4 produced twice as many piliated cells, attached in 2.5-fold-higher numbers to soybean root segments, and colonized roots in about 2-fold-higher numbers than did the parental strain, 110 ARS. Mutants CFK35 and CFK38 were reduced in their attachment about 2-fold and 3.5-fold, respectively. This corresponded to reductions in piliated cells in their populations, reduced reaction with anti-pilus antiserum, and reduced hydrophobic attachment. Mutants CFK4 and CFK38 nodulated soybeans at about the same level as the parent strain, but CFK35 induced only pseudonodules. Two-dimensional gel analyses of the proteins from the mutants showed relatively few changes in proteins. 相似文献
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Carolyn M. Giles Beatrice Uring-Lambert Wolfgang Boksch Margot Braun Joelle Goetz Rainer Neumann Gottfried Mauff Georges Hauptmann 《Human genetics》1987,77(4):359-365
Summary The finding of two duplicated C4A haplotypes in a normal French family led to a detailed study of their C4 polymorphism. The father had an extremely rare A*6A*11, B* QO haplotype inherited by all of his children and the mother had the more common A*3A*2, B*QO haplotype. Two HLA identical daughters only have four C4A alleles. The father's A11 allotype expresses Ch: 1 (Chido) rather than Rg:1 (Rodgers) and represents a new Ch phenotype Ch: 1,-2,-3,-4,-5,-6. In order to clarify the genetic background in this unusual family, DNA studies of restriction fragment length polymorphisms (RFLPs) were undertake. The father's rare haplotype, which expresses two C4A allotypes, results from a long and a short C4 gene normally associated with the A*6, B*1 that also exhibits the BglII RFLP. As it travels in an extended MHC haplotype HLA A2, B57 (17), C2*C, BF*S, DR7 that is most frequently associated with A*6, B*1, we postulate that the short C4B has been converted in the chain region to a C4A gene which produces a C4A protein. This report of a short C4A gene is the first example in the complex polymorphism of C4. 相似文献
27.
Summary Nine independent mutants which are supersensitive (ssl
–) to G1 arrest by the mating hormone a-factor were isolated by screening mutagenized Saccharomyces cerevisiae MAT cells on solid medium for increased growth inhibition with a-factor. These mutants carried lesions in two complementation groups, ssl1 and ssl2. Mutations at the ssl1 locus were mating type specific: MAT ssl1
– cells were supersensitive to -factor but MAT ssl1
– were not supersensitive to -factor. In contrast, mutations at the ssl2. locus conferred supersensitivity to the mating hormone of the opposite mating type on both MAT, and MATa cells. The -cell specific capacity to inactivate externally added a-factor was shown to be lacking in MAT ssl1
– mutants whereas MAT ssl2. cells were able to inactivate a-factor. Complementation analysis showed that ssl2 and sst2, a mutation originally isolated as conferring supersensitivity to -factor to MATa cells, are lesions in the same gene. The ssl1 gene was mapped 30.5 centi-Morgans distal to ilv5 on chromosome XII. 相似文献
28.
Helmut Tr?ster Wolfgang Kissel Michael F. Trendelenburg Ansgar Hofmann 《Molecular & general genetics : MGG》1989,217(2-3):533-535
Summary Eight representative recombinant background clones of λEMBL3 were analysed usingKpnI,BamHI,SalI,EcoRI andHindIII digestion. We found that λEMBL3 carries its own left arm in theBamHI cloning site. In this way, recombinant molecules were found to be generated which can grow onEscherichia coli strain NM539. In all cases analysed, the left arm DNA was inserted in a head to tail orientation. Seven clones carried a
restoredBamHI site at thecos site-BamHI site connection. In the region where the inserted left arm and the right arm were ligated,BamHI cloning produces a large palindromic sequence consisting of two polylinkers. ThisBamHI site was incompletely cleaved in all cases analysed. We assume that a part of the λ DNA molecule in this region shows a
cruciform structure prohibiting recognition or cleavage of this site by restriction endonucleaseBamHI. 相似文献
29.
A mutant rat major histocompatibility haplotype showing a large deletion of class I sequences 总被引:2,自引:2,他引:0
The LEW.1LM1 inbred rat strain, which has been derived from a (LEW×LEW.1W) F2 hybrid, carries a major histocompatibility (RT1) haplotype which is distinct from that of the LEW strain (RT1
1) in that certainRT1.C region-determined class I antigens are not expressed. Here we show that this phenotypic defect is due to genomic deletion
of about 100 kb of theRT1.C region. Certain deleted DNA fragments have been cloned from the wild-type DNA into the EMBL4 vector. Five clones have been
characterized and are shown to possess different restriction maps and to each carry a single stretch of class I cross-hybridizing
sequences. Probes derived from the non-class I coding part of two clones detect fragments which are present in the wild-type
but absent from thelm1 mutant. The type of deletion described here in the rat is discussed in the context ofH-2D/Q deletions in the mouse. 相似文献
30.