Chitin amendment is an agricultural management strategy for controlling soil-borne plant disease. We previously reported an exponential decrease in chitin added to incubated upland soil. We herein investigated the transition of the bacterial community structure in chitin-degrading soil samples over time and the characteristics of chitinolytic bacteria in order to elucidate changes in the chitinolytic bacterial community structure during chitin degradation. The addition of chitin to soil immediately increased the population of bacteria in the genus Streptomyces, which is the main decomposer of chitin in soil environments. Lysobacter, Pseudoxanthomonas, Cellulosimicrobium, Streptosporangium, and Nonomuraea populations increased over time with decreases in that of Streptomyces. We isolated 104 strains of chitinolytic bacteria, among which six strains were classified as Lysobacter, from chitin-treated soils. These results suggested the involvement of Lysobacter as well as Streptomyces as chitin decomposers in the degradation of chitin added to soil. Lysobacter isolates required yeast extract or casamino acid for significant growth on minimal agar medium supplemented with glucose. Further nutritional analyses demonstrated that the six chitinolytic Lysobacter isolates required methionine (Met) to grow, but not cysteine or homocysteine, indicating Met auxotrophy. Met auxotrophy was also observed in two of the five type strains of Lysobacter spp. tested, and these Met auxotrophs used d-Met as well as l-Met. The addition of Met to incubated upland soil increased the population of Lysobacter. Met may be a factor increasing the population of Lysobacter in chitin-treated upland soil.
SummaryRecently, a diet enriched in oleate and moderately restricted in hexacosanoate (C26:0) was found effective to reduce the plasma very long chain fatty acid (VLCFA) levels in patients with adrenoleukodys trophy (ALD), an X-linked disorder characterized by demyelination of the adrenal cortex and cerebral white matter, and accumulation of saturated VLCFA, particularly 026:0, in tissues of the demyelination. The infor mation about the C26:0 content in Japanese food was, however, almost nil except for one report about foods in the USA, but this did not include some Japanese common foods. With the hope of treating an ALD patient in our hospital, 026:0 contents in Japanese common foods (42 items) were measured. In our case, a one-hour direct transesterification method was used to obtain methylesters of total fatty acids in foods and they were applied directly to a selected ion monitoring gas chromatography-mass spectrometry for the quantitative C26:0 analysis. The C26:0 content in nuts and seeds as well as in fats and oils was found to be significantly higher than in other foods; the content was highest in peanuts. The content in almost all kinds of examined fishes, the common protein foods in Japan, was relatively low. From these data and that in the national nutrition survey in 1986, the daily intake of C26:0 from the average Japanese diet could be estimated to be 12-36mg. It can be recommended, therefore, that nuts and seeds as well as fats and oils should be restricted as severely as possible from the diet of ALD patients in Japan in order to keep daily C26:0 intake below 10mg as recommended in the USA.
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