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  • 1
    Electronic Resource
    Electronic Resource
    Experimental genome evolution: large-scale genome rearrangements associated with resistance to replacement of a chromosomal restriction–modification gene complex (2001)
    Oxford, UK : Blackwell Science, Ltd
    Molecular microbiology 40 (2001), S. 0 
    Details
    ISSN: 1365-2958
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Biology , Medicine
    Notes: Type II restriction enzymes are paired with modification enzymes that protect type II restriction sites from cleavage by methylating them. A plasmid carrying a type II restriction–modification gene complex is not easily replaced by an incompatible plasmid because loss of the former leads to cell death through chromosome cleavage. In the present work, we looked to see whether a chromosomally located restriction–modification gene complex could be replaced by a homologous stretch of DNA. We tried to replace the PaeR7I gene complex on the Escherichia coli chromosome by transducing a homologous stretch of PaeR7I-modified DNA. The replacement efficiency of the restriction–modification complex was lower than expected. Some of the resulting recombinant clones retained the recipient restriction–modification gene complex as well as the homologous DNA (donor allele), and slowly lost the donor allele in the absence of selection. Analysis of their genome-wide rearrangements by Southern hybridization, inverse polymerase chain reaction (iPCR) and sequence determination demonstrated the occurrence of unequal homologous recombination between copies of the transposon IS3. It was strongly suggested that multiple rounds of unequal IS3–IS3 recombination caused large-scale duplication and inversion of the chromosome, and that only one of the duplicated copies of the recipient PaeR7I was replaced.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1365-2958.2001.02436.x
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  • 2
    Electronic Resource
    Electronic Resource
    Characterization of the Neurospora crassa mus-25 mutant: the gene encodes a protein which is homologous to the Saccharomyces cerevisiae Rad54 protein (2000)
    Springer
    Molecular genetics and genomics 264 (2000), S. 154-163 
    Details
    ISSN: 1617-4623
    Keywords: Neurospora crassa mus-25 Recombinational repair Rad54p SNF2 family
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract. Characterization of the Neurospora crassa mus-25 mutant suggests that it is defective in recombination repair and belongs to the uvs-6 epistasis group. It shows a high sensitivity to the alkylating agents methyl methanesulfonate (MMS) and N-methyl-N'-nitro-N-nitrosoguanidine (MNNG), but not to UV radiation. It is barren (i.e. does not produce ascospores) in homozygous crosses. The frequency of MMS-induced mutations at the ad-3 loci is approximately three times higher than in the wild type. The ratio of homologous to non-homologous integration of the pMTR::HYG plasmid is much lower than in wild type. The mus-25 mutant is epistatic to the mei-3 mutant for MMS sensitivity. mei-3, which is a homololog of the Saccharomyces cerevisiae gene RAD51, is a member of the uvs-6 epistasis group which contains several genes that are homologous to recombination repair genes in other organisms. The mus-25 gene was cloned by identifying a genomic DNA fragment which complements the MMS sensitivity of the mutant. The amino acid sequence deduced from the cloned DNA showed a high degree of homology to the Rad54 protein, which is involved in recombinational repair in S. cerevisiae. Comparison of the nucleotide sequences of the genomic and cDNAs of the mus-25 gene revealed an ORF of 2505 bp with a single 118-bp intron beginning immediately after the second nucleotide of the AUG start codon. The molecular weight of the deduced gene product was 93.5 kDa. The transcript level was raised within 60 min after UV irradiation or MMS treatment, as also observed for the expression of the other N. crassa recombinational repair genes, suggesting the existence of a common mechanism which induces expression of the recombinational repair genes in response to DNA damage.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004380000303
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  • 3
    Electronic Resource
    Electronic Resource
    Heart transplantation for radiation-associated end-stage heart failure (2000)
    Springer
    Transplant international 13 (2000), S. 162-165 
    Details
    ISSN: 1432-2277
    Keywords: Key words Radiation-induced heart disease ; Heart transplantation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Radiation-induced heart disease is an increasingly recognized late sequela of mediastinal radiation therapy for malignant neoplasms. We report four cases of heart transplantation for end-stage heart failure induced by mediastinal radiation therapy. Short-term and intermediate-term results are excellent with all four patients currently surviving a mean of 48 months after transplantation. Neither a second malignancy nor recurrence of the primary malignancy has been observed to date. The early results of heart transplantation for end-stage, radiation-induced heart disease are encouraging.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001470050679
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