Browsing by Author "KIRK, TK"

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    CHANGES IN MOLECULAR-SIZE DISTRIBUTION OF CELLULOSE DURING ATTACK BY WHITE ROT AND BROWN ROT FUNGI
    (AMER SOC MICROBIOLOGY, 1992) KLEMANLEYER, K; AGOSIN, E; CONNER, AH; KIRK, TK
    The kinetics of cotton cellulose depolymerization by the brown rot fungus Postia placenta and the white rot fungus Phanerochaete chrysosporium were investigated with solid-state cultures. The degree of polymerization (DP; the average number of glucosyl residues per cellulose molecule) of cellulose removed from soil-block cultures during degradation by P. placenta was first determined viscosimetrically. Changes in molecular size distribution of cellulose attacked by either fungus were then determined by size exclusion chromatography as the tricarbanilate derivative. The first study with P. placenta revealed two phases of depolymerization: a rapid decrease to a DP of approximately 800 and then a slower decrease to a DP of approximately 250. Almost all depolymerization occurred before weight loss. Determination of the molecular size distribution of cellulose during attack by the brown rot fungus revealed single major peaks centered over progressively lower DPs. Cellulose attacked by P. chrysosporium was continuously consumed and showed a different pattern of change in molecular size distribution than cellulose attacked by P. placenta. At first, a broad peak which shifted at a slightly lower average DP appeared, but as attack progressed the peak narrowed and the average DP increased slightly. From these results, it is apparent that the mechanism of cellulose degradation differs fundamentally between brown and white rot fungi, as represented by the species studied here. We conclude that the brown rot fungus cleaved completely through the amorphous regions of the cellulose microfibrils, whereas the white rot fungus attacked the surfaces of the microfibrils, resulting in a progressive erosion.
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    METABOLISM OF LIGNIN MODEL COMPOUNDS OF THE ARYLGLYCEROL-BETA-ARYL ETHER TYPE BY PSEUDOMONAS-ACIDOVORANS D3
    (1987) VICUNA, R; GONZALEZ, B; MOZUCH, MD; KIRK, TK
    A natural bacterial isolate that we have classified as Pseudomonas acidovorans grows on the lignin model compounds 1-(3,4-dimethoxyphenyl)-2-(2-methoxyphenoxy)propane-1,3-diol (compound 1) and 1-(4-hydroxy-3-methoxyphenyl)-2-(2-methoxyphenoxy)propane-1,3-diol (compound 1''), as well as on the corresponding 1-oxo compounds (2 and 2'') as sole sources of carbon and energy. Metabolic intermediates present in cultures growing on compound 1 included compound 2,2-methoxyphenol (guaiacol [compound 3]), .beta.-hydroxypropioveratrone (compound 4), acetoveratrone (compound 5), and veratric acid (compound 6). Also identified were compounds 1'', 2'', .beta.-hydroxypropiovanillone (compound 4''), and acetovanillone (compound 5''), indicating that 4-O demethylation also occurs. The phenolic intermediates were the same as those found in cultures growing on compound 1''. Compounds 2 and 2'' were in part also reduced to compounds 1 and 1'', respectively. Compound 3 was shown to be derived from the 2-methoxyphenoxy moiety. A suggested degradation scheme is as follows: compound 1 .fwdarw. 2 .fwdarw. (3 + 4) .fwdarw. 5 .fwdarw. 6 (and similarly for 1''). In this scheme, the key reaction is cleavage of the ether linkage between C-2 (C.beta.) of the phenylpropane moiety and the 2-methoxyphenoxy moiety in compounds 2 and 2'' (i.e., .beta.-aryl ether cleavage). On the basis of compounds identified, viz., 3 and 4 (4''), cleavage appears formally to be reductive. Because this is unlikely, the initial cleavage products probably were not detected. The implications of these results for the enzyme(s) responsible are discussed.