High-throughput sequencing was applied to compare the intestinal microbiota in largemouth bronze gudgeon either healthy or affected by furunculosis. Proteobacteria, Actinobacteria, Tenericutes, Firmicutes and Bacteroidetes were detected as the predominant bacterial phyla in the gut of both diseased and healthy fish. The abundance of Proteobacteria differed significantly between the two groups of fish, mainly due to the overwhelming prevalence of Aeromonas in the diseased fish (81% ± 17%), while the genus was unevenly spread among the apparently healthy fish (33% ± 33%). The bacterial diversity in the intestine of diseased fish was markedly lower than in healthy fish. Analysis revealed the significant dissimilarity between the gut microbiota of diseased and healthy fish. The bacterial profiles in the gut were further characterized with the 28 phylotypes that were shared by the two groups. In diseased fish, two shared OTUs (OTU0001 and OTU0013) were closely related to Aeromonas salmonicida, their total proportion exceeding 70% of the sequences in diseased fish, while averaging 5.2% ± 4.6% in the healthy fish. This result suggested the presence of healthy carriers of pathogenic A. salmonicida among the farmed fish, and the gut appeared as a probable infection source for furunculosis in largemouth bronze gudgeon.

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Two strains of Aeromonas salmonicida, YK and BG, were isolated from largemouth bronze gudgeon and northern whitefish in China, and identified as A. salmonicida subsp. salmonicida based on phylogenetic analysis of vapA and 16S rRNA gene sequences. YK and BG originated from freshwater fish, one of which belonged to the cyprinid family, and the strains showed a difference in virulence. Subsequently, we performed whole genome sequencing of the strains, and comparison of their genomic sequences to the genome of the A449 reference strain revealed various genomic rearrangements, including a new variant of the genomic island AsaGEI in BG, designated as AsaGEI2c This is the first report on a GEI of A. salmonicida strain from China. Furthermore, both YK and BG strains contained a Tn7 transposon inserted at the same position in the chromosome. Finally, IS-dependent rearrangements on pAsa5 are deemed likely to have occurred, with omission of the resD gene in both strains as well as omission of genes related to the IncF conjugal transfer system in the YK isolate. This study demonstrates that A. salmonicida subsp. salmonicida can infect non-salmonids (cyprinids) in addition to salmonids, and that AsaGEI2c might be useful as a geographical indicator of Chinese A. salmonicida subsp. salmonicida isolates.

Sphingosine 1-phosphate (S1P), a potent bioactive phospholipid, has been reported to regulate a broad spectrum of biological processes. However, little is known regarding S1P's effects on mitochondrial function. In this study, we investigated the S1P's effects on the Peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α) signaling pathway and mitochondrial biogenesis in Hep G2 cells. Our results indicate that administration of S1P leads to a significant upregulation of mitochondrial DNA replication and transcription, increased mitochondrial mass, and elevated adenosine triphosphate synthesis. In addition, we found that treatment with S1P stimulates expression of PGC-1α, a master regulator of mitochondrial biogenesis, as well as its downstream targets: nuclear respiratory factor 1 (NRF1) and mitochondrial transcription factor A (TFAM). Moreover, our data demonstrate that S1P's effects on PGC-1α and mitochondrial biogenesis are mediated by the protein kinase A/cAMP response element-binding protein (PKA/CREB) pathway. Importantly, we also revealed that S1P's effects on mitochondrial biogenesis are dependent on its type 2 receptor (S1P2), though not on either its type 1 (S1P1) or type 3 (S1P3) receptors. Based on these observations, we concluded that S1P activates the PKA/CREB pathway through S1P2, which then promotes expression of PGC-1α/NRF1/TFAM and subsequent mitochondrial biogenesis in Hep G2 cells.

The complete mitochondrial genome for Gymnocypris eckloni and Gymnocypris przewalskii ganzihonensis is 16,686 and 16,682 bp in size, respectively. Both of the mitochondrial genomes have identical genomic organization and structure including 13 protein-coding genes (PCGs), 22 tRNA genes, 2 rRNA genes and 1 control region as found in other vertebrates, with the exception of 86 bp non-coding nucleotides between tRNA(Thr) and tRNA(Pro). The phylogenetic analyses based on the concatenated nucleotide sequence of 12 PCGs on the heavy strand supported a relatively closed relationship among G. eckloni, G. p. przewalskii and G. p. ganzihonensis. The sequence divergence between G. eckloni and G. przewalskii, as well as within G. przewalskii, is relatively low compared to the average sequence divergence among other cyprinid fishes, suggesting that they are the most closely related species resulted from a relatively recent speciation event. The estimated molecular divergence time is coincided with a relatively recent speciation event occurring during the separation of the Yellow River and Qinghai Lake.

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Increasing lines of evidence indicate the role of long non-coding RNAs (LncRNAs) in gene regulation and tumor development. Hence, it is important to elucidate the mechanisms of LncRNAs underlying the proliferation, metastasis, and invasion of lung adenocarcinoma (LUAD). We employed microarrays to screen LncRNAs in LUAD tissues with and without lymph node metastasis and revealed their effects on LUAD. Among them, Linc00426 was selected for further exploration in its expression, the biological significance, and the underlying molecular mechanisms. Linc00426 exhibits ectopic expression in LUAD tissues and cells. The ectopic expression has been clinically linked to tumor size, lymphatic metastasis, and tumor differentiation of patients with LUAD. The deregulation of Linc00426 contributes to a notable impairment in proliferation, invasion, metastasis, and epithelial–mesenchymal transition (EMT) in vitro and in vivo. Mechanistically, the deregulation of Linc00426 could reduce cytoskeleton rearrangement and matrix metalloproteinase expression. Meanwhile, decreasing the level of Linc00426 or increasing miR-455-5p could down-regulate the level of UBE2V1. Thus, Linc00426 may act as a competing endogenous RNA (ceRNA) to abate miR-455-5p-dependent UBE2V1 reduction. We conclude that Linc00426 accelerates LUAD progression by acting as a molecular sponge to regulate miR-455-5p, and may be a potential novel tumor marker for LUAD.