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Articles 61 - 62 of 62
Full-Text Articles in Genetics and Genomics
Characterization Of Experimentally Induced, Nonaflatoxigenic Variant Strains Of Aspergillus Parasiticus., Shubha Kale Ireland, J. W. Cary, D. Bhatnagar, J. W. Bennett
Characterization Of Experimentally Induced, Nonaflatoxigenic Variant Strains Of Aspergillus Parasiticus., Shubha Kale Ireland, J. W. Cary, D. Bhatnagar, J. W. Bennett
Faculty and Staff Publications
Six previously isolated, nonaflatoxigenic variants of Aspergillus parasiticus, designated sec mutants, were characterized morphologically by electron microscopy, biochemically by biotransformation studies with an aflatoxin precursor, and genetically by Northern (RNA) hybridization analysis of aflatoxin biosynthetic gene transcripts. Scanning electron micrographs clearly demonstrated that compared with the parental sec+ forms, the variant sec forms had an abundance of vegetative mycelia, orders of magnitude reduced number of conidiophores and conidia, and abnormal metulae. Conidiospores were detected in sec cultures only at higher magnifications (x500), in contrast to the sec+ (wild-type) strain, in which abundant conidiospores (masking the vegetative mycelia) were observed even …
Cole1 Copy Number Mutants., Londa Schmidt, Joseph Inselburg
Cole1 Copy Number Mutants., Londa Schmidt, Joseph Inselburg
Dartmouth Scholarship
A deletion mutant of the colicin E1-derived plasmid, pDMS6642, exhibited an approximately fourfold increase in copy number. We subsequently isolated hydroxylamine-induced mutants of that plasmid that had a further increase in copy number. Analysis of them suggests that the increased copy number of pDMS6642 is associated with transcriptional readthrough from a Tn3 transposon into the region of ColE1 containing information that influences plasmid replication. The hydroxylamine mutation in one copy number mutant appeared to increase the plasmid copy number by stimulating readthrough transcription from the Tn3 transposon into the ColE1 replication control region, whereas the other hydroxylamine mutation acts by …