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Higher plants efficiently conserve energy ATP in cellulose biosynthesis by expression of sucrose synthase, in which the high free energy between glucose and fructose in sucrose can be conserved and used for the synthesis of UDP-glucose. A mixture of sucrose synthase and bacterial cellulose synthase proceeded to form UDP-glucose from sucrose plus UDP and to synthesize 1,4-␤-glucan from the sugar nucleotide. The mutant sucrose synthase, which mimics phosphorylated sucrose synthase, enhanced the reaction efficiency (V max ͞K m ) on 1,4-␤-glucan synthesis, in which the incorporation of glucose from sucrose was increased at low concentrations of UDP. Because UDP formed after glucosyl transfer can be directly recycled with sucrose synthase, UDPglucose formed appears to show high turnover with cellulose synthase in the coupled reaction. The expression of sucrose synthase in Acetobacter xylinum not only changed sucrose metabolism but also enhanced cellulose production, in which UDP-glucose was efficiently formed from sucrose. Although the level of UDP-glucose in the transformant with mutant sucrose synthase cDNA was only 1.6-fold higher than that in plasmid-free cells, the level of UDP was markedly decreased in the transformant. The results show that sucrose synthase serves to channel carbon directly from sucrose to cellulose and recycles UDP, which prevents UDP build-up in cellulose biosynthesis.

A bacterial strain, designated AST4T, was isolated from activated sludge. The bacterium did not show significant growth on nutrient broth, but growth was clearly stimulated by addition of supernatant from other bacterial cultures. Culture filtrate of a strain related to the genus Sphingomonas in particular increased the cell yield and growth rate of strain AST4T. Phylogenetic analysis based on the 16S rRNA gene sequences showed that strain AST4T is located within the ‘Rhodobacter group’ in the α-3 subclass of Proteobacteria, but is clearly distant from related genera in this group such as Paracoccus, Rhodobacter and Rhodovulum. Strain AST4T is a Gram-negative, non-motile, rod-shaped (0·6–0·8×1·3–2·0 μm) and aerobic bacterium. It was not able to reduce nitrate to nitrite or N2. No phototrophic growth was observed. Optimal growth occurred at 30 °C and pH 6·5–7·5. The dominant cellular fatty acid in the isolate was C18 : 1 cis11. Ubiquinone-10 was the major respiratory quinone. The G+C content was 64·5 mol% (by HPLC). Based on the phylogenetic and phenotypic traits, the name Catellibacterium nectariphilum gen. nov., sp. nov. is proposed for this isolate; the type strain is AST4T (=NBRC 100046T=JCM 11959T=DSM 15620T).

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The effects of eel atrial natriuretic peptide (ANP) on drinking were investigated in eels adapted to freshwater (FW) or seawater (SW) or in FW eels whose drinking was stimulated by a 2-ml hemorrhage. An intra-arterial infusion of ANP (0.3–3.0 pmol ⋅ kg−1 ⋅ min−1), which increased plasma ANP level 1.5- to 20-fold, inhibited drinking dose dependently in all groups of eels. The drinking rate recovered to the level before ANP infusion within 2 h after infusate was replaced by saline. The inhibition at 3.0 pmol ⋅ kg−1 ⋅ min−1was profound in FW eels and hemorrhaged FW eels, whereas significant drinking still remained after inhibition in SW eels. Plasma ANG II concentration also decreased dose dependently during ANP infusion and recovered to the initial level after saline infusion in all groups of eels. The decrease at 3.0 pmol ⋅ kg−1 ⋅ min−1was large in FW eels and hemorrhaged FW eels compared with that of SW eels. Thus the changes in drinking rate and plasma ANG II level were parallel during ANP infusion. Plasma sodium concentration and osmolality decreased during ANP infusion in SW and FW eels, and they were restored after saline infusion. In hemorrhaged FW eels, however, ANP infusion did not alter plasma sodium concentration and osmolality. Hematocrit did not change during ANP infusion in any group of eels. Collectively, ANP infusion at physiological doses decreased drinking rate and plasma ANG II concentration in parallel in both FW and SW eels. It remains undetermined whether the inhibition of drinking is caused by direct action of ANP or through inhibition of ANG II, which is known as a potent dipsogen in all vertebrate species, including eels.

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