Nitrate assimilation in rice seedlings as affected by mineral nutrition

Deficiencies of each macronutrient (N, P, K, Ca, Mg and Fe)in the culture solution depressed the specific activities ofnitrate reductase (NR) and nitrite reductase (NiR) from riceseedlings. Nitrate and potassium deficiencies especially loweredNR induction, whereas phosphorus deficiency caused the leastdecrease in enzyme induction. On the other hand the activityof NiR was decreased most by deficiencies of nitrate and phosphorus.Potassium deficiency was not as effective in suppressing theinduction of NiR. Sulfur deficiency slightly promoted the inductionof both NR and NiR. Generally, micronutrient deficiencies didnot affect either enzyme. NR induction was slightly decreasedby B, Zn, Cu and Mo deficiencies, and increased by Mn deficiency;whereas NiR activity was slightly increased by B and Cu deficiencies,and was not affected by other micronutrients. Nitrate contentwas decreased by deficiencies of N, P, K, Ca, and micronutrients,and unaffected by Mg, Fe and S deficiencies. Glutamic acid dehydrogenase(GDH) activity was increased by N, Fe and P deficiencies, anddecreased by Mo and Zn deficiencies, and unaffected by othernutrient treatments. (Received August 25, 1976; )     

Virulence-associated chromosomal loci of Shigella flexneri identified by random Tn5 insertion mutagenesis

Shigellae are the causative agents of bacillary dysentery and are capable of invading epithelial cells, multiplying therein and spreading into adjacent cells. To identify genes on the chromosome associated with the virulence phenotype, 9114 independent Tn5 insertion mutants were isolated in a virulent strain of Shigella flexneri. By using an in vitro assay for intercellular spread or an animal infection model, the Serény test, 50 chromosomal Tn5 mutants with reduced virulence were identified. The 50 mutants were characterized with respect to their virulence phenotypes, including three different mutations that affect invasion of epithelial cells, bacterial metabolism and structure of lipopolysaccharide. Mutants with reduced invasive ability were further characterized and it was found that two of them had decreased levels of IpaB, C and D antigens as well as the mRNA for the ipaBCD operon encoded by the large virulence plasmid, suggesting that positive regulatory elements for the ipaBCD operon are encoded by the chromosome. Assignment of the 50 Tn5 insertions of the mutants to the 19 NotI restriction fragments of the chromosomal DNA has permitted the identification of at least nine virulence-associated chromosomal loci.     

Construction of NotI restriction map of the Streptococcus mutans genome

Streptococcus mutans and Streptococcus sobrinus are the major causative organisms of human dental caries. Pulsed-field gel electrophoresis (PFG) showed that the restriction enzyme NotI produced ten and six DNA fragments from the genomes of S. mutans strain MT8148 and S. sobrinus strain 6715, respectively. The sizes of the chromosomes of S. mutans and S. sobrinus were each estimated to be about 2200 kb. The NotI restriction map of S. mutans MT8148 genome was constructed by Southern blot analysis with probes that overlapped two adjacent NotI fragments. Several virulence-associated genes of S. mutans were placed on the NotI restriction map. In addition, unique 'fingerprints' of S. mutans chromosomal DNA digested with NotI were produced by PFG, and these may be useful for epidemiological studies.     

Molecular cloning and characterization of chromosomal virulence region kcpA of Shigella flexneri

In Shigella flexneri, in addition to several well-recognized plasmid-borne virulence loci, at least three genetic loci implicated in pathogenesis have been recognized on the chromosome. To understand more about the pathogenesis of bacillary dysentery at a molecular level, the genetically recognized but previously unidentified KcpA region (one of the chromosomal regions near purE) was cloned and sequenced. A single translatable open reading frame encoding a 12310 Dalton protein corresponding to the minicell product was found. Immunofluorescence microscopy, as well as optical and electron microscopic comparison of tissue-cultured cells and guinea-pigs' eyes infected with wild-type or kcpA mutant bacteria, revealed that the kcpA product is required by invading bacteria for spread into adjacent cells.     

Regions associated with the stable maintenance of plasmid pSC101 and its tetracycline resistance

Summary Two regions tentatively called unsA and unsR were identified on pSC101. One, unsA, corresponds to less than 650 bp of the N-terminal in the tetracycline resistance structural gene and seems to inhibit stable maintenance of pSC101. The other, unsR, is defined within the 1 kb XhoI-EcoRI region located upstream of the tetracycline resistance structural gene and is a regulatory gene clearly distinct from tetR (Unger et al. 1984); it serves as a suppressor of the unsA function.