c Mortierella alpina is a filamentous fungus commonly found in soil that is able to produce lipids in the form of triacylglycerols that account for up to 50% of its dry weight. Analysis of the M. alpina genome suggests that there is a phenylalanine-hydroxylating system for the catabolism of phenylalanine, which has never been found in fungi before. We characterized the phenylalanine-hydroxylating system in M. alpina to explore its role in phenylalanine metabolism and its relationship to lipid biosynthesis. Significant changes were found in the profile of fatty acids in M. alpina grown on medium containing an inhibitor of the phenylalanine-hydroxylating system compared to M. alpina grown on medium without inhibitor. Genes encoding enzymes involved in the phenylalanine-hydroxylating system (phenylalanine hydroxylase [PAH], pterin-4␣-carbinolamine dehydratase, and dihydropteridine reductase) were expressed heterologously in Escherichia coli, and the resulting proteins were purified to homogeneity. Their enzymatic activity was investigated by high-performance liquid chromatography (HPLC) or visible (Vis)-UV spectroscopy. Two functional PAH enzymes were observed, encoded by distinct gene copies. A novel role for tetrahydrobiopterin in fungi as a cofactor for PAH, which is similar to its function in higher life forms, is suggested. This study establishes a novel scheme for the fungal degradation of an aromatic substance (phenylalanine) and suggests that the phenylalaninehydroxylating system is functionally significant in lipid metabolism.
l-Arabinose is a monosaccharide extracted from plants
or fibers, which is known to have a variety of functional properties.
In this study, we aim to investigate whether l-arabinose
could inhibit colitis by modulating gut microbiota. l-Arabinose
was administered in mice daily in a dextran sodium sulfate (DSS)-induced
colitis model. The histological analysis, disease index, and the expression
of inflammatory genes were measured. 16S-rRNA sequence analysis was
performed to investigate gut microbiota. Intriguingly, we found that l-arabinose could repress DSS-induced colitis and inhibit p38-/p65-dependent
inflammation activation. Besides that, our data revealed that l-arabinose-modulated DSS-induced gut microbiota were disturbed.
Additionally, the perturbed gut microbiota was responsible for the
suppressive effects of l-arabinose on DSS-induced colitis
treated with antibiotics. Lastly, Caco-2 cells were used to confirm
the protective effects of l-arabinose in colitis or inflammatory
bowel disease. As expected,
the protein expression levels in Caco-2 cells of pro-inflammatory
genes, which were treated with l-arabinose and incubated
with or without tumor necrosis factor alpha. Our work suggested that l-arabinose exerts anti-inflammation effects in DSS-induced
colitis. These beneficial effects have correlations with the composition,
diversity, and abundance of the gut microbiota regulated by l-arabinose. l-Arabinose could be a remarkable candidate
as a functional food or novel therapeutic strategy for intestinal
health.
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