Berberis koreana is a medicinal plant containing berberine, which is a bioactive compound of the benzylisoquinoline alkaloid (BIA) class. BIA is widely used in the food and drug industry for its health benefits. To investigate the berberine biosynthesis pathway, gene expression analysis was performed in leaves, flowers, and fruits at different stages of growth. This was followed by full-length cDNA sequencing analysis using the PacBio sequencer platform to determine the number of isoforms of those expressed genes. We identified 23,246 full-length unigenes, among which 8,479 had more than one isoform. The number of isoforms ranged between two to thirty-one among all genes. Complete isoform analysis was carried out on the unigenes encoding BIA synthesis. Thirteen of the sixteen genes encoding enzymes for berberine synthesis were present in more than one copy. This demonstrates that gene duplication and translation into isoforms may contribute to the functional specificity of the duplicated genes and isoforms in plant alkaloid synthesis. Our study also demonstrated the streamlining of berberine biosynthesis via the absence of genes for enzymes of other BIAs, but the presence of all the genes for berberine biosynthesize in B. koreana. In addition to genes encoding enzymes for the berberine biosynthesis pathway, the genes encoding enzymes for other BIAs were not present in our dataset except for those encoding corytuberine synthase (CTS) and berbamunine synthase (BS). Therefore, this explains how B. koreana produces berberine by blocking the pathways leading to other BIAs, effectively only allowing the pathway to lead to berberine synthesis.

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The fungus Daldinia childiae strain JS-1345, isolated from stem tissue of Abies koreana (Korean fir), has shown strong anti-inflammatory activity. Here, we report the genome sequence of D. childiae JS-1345. The final assembly consisted of 133 scaffolds totaling 38,652,569 bp (G+C content, 44.07%).

Peroxynitrite is a potent neurotoxic molecule produced from a reaction between NO and superoxide and induces NO-mediated inflammation under neuropathological conditions. Previously, we reported that glucose deprivation induced ATP depletion and cell death in immunostimulated astrocytes, which was mainly due to peroxynitrite. In this study, the role of MAPKs (ERK1/2, p38MAPK, and JNK1SAPK) signal pathway in the SIN-1/glucose deprivation-induced death of astrocytes was examined. A combined treatment with glucose deprivation and 50 microM SIN-1, an endogenous peroxynitrite generator, rapidly and markedly increased the death in rat primary astrocytes. Also, SIN-1/glucose deprivation resulted in the activation of MAPKs, which was significantly blocked by the treatment with 20 microM MAPKs inhibitors (ERK1/2, PD98059; p38MAPK, SB203580; JNK/SAPK, SP600125). Interestingly, SIN-1/glucose deprivation caused the loss of intracellular ATP level, which was significantly reversed by MAPKs inhibitors. These results suggest that the activation of MAPKs plays an important role in SIN-1/glucose deprivation-induced cell death by regulating the intracellular ATP level.

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