Isolation, identification, and histopathological analysis of Vibrio tubiashii from lined seahorse Hippocampus erectus.

The lined seahorse Hippocampus erectus is an economically important aquaculture species; however, the low survival rate of juvenile seahorses severely restricts their large-scale cultivation. According to previous research, dead juvenile seahorses (4-6 cm) showed symptoms of suspected enteritis, including abdominal depression, raised cloaca, partial hepatic congestion, and yellow sticky liquid filling the intestine. Here, we isolated a Gram-negative bacterium from diseased juvenile seahorses and tentatively named the strain HEL-5. Healthy juvenile seahorses were then challenged with the strain through intraperitoneal injection, with results confirming that HEL-5 was pathogenic for seahorses at a median lethal dose of 5.81 × 105 CFU g-1 fish weight. Based on morphological observations, biochemical characteristics, and sequence analysis of 16S rRNA and housekeeping genes (gyrB, ftsZ, and gapA), we identified HEL-5 as Vibrio tubiashii. Histopathological observations revealed that V. tubiashii was capable of causing lytic necrosis of hepatocytes and forming obvious necrotic foci, and renal pathology was characterized by tubular collapse and tubular epithelial-cell shedding into the lumen accompanied by a large number of inflammatory cells infiltrating the tissues of the intestines and kidneys. Antimicrobial-susceptibility testing showed that the strain was highly sensitive to macrolides, chloramphenicol, sulfonamides, aminoglycosides, and cephalosporins. These findings represent the first report of isolation of V. tubiashii from diseased juvenile seahorses and provide a foundation for the prevention and treatment of vibrio disease in seahorse aquaculture.

Loss of Myomixer Results in Defective Myoblast Fusion, Impaired Muscle Growth, and Severe Myopathy in Zebrafish.

The development and growth of fish skeletal muscles require myoblast fusion to generate multinucleated myofibers. While zebrafish fast-twitch muscle can fuse to generate multinucleated fibers, the slow-twitch muscle fibers remain mononucleated in zebrafish embryos and larvae. The mechanism underlying the fiber-type-specific control of fusion remains elusive. Recent genetic studies using mice identified a long-sought fusion factor named Myomixer. To understand whether Myomixer is involved in the fiber-type specific fusion, we analyzed the transcriptional regulation of myomixer expression and characterized the muscle growth phenotype upon genetic deletion of myomixer in zebrafish. The data revealed that overexpression of Sonic Hedgehog (Shh) drastically inhibited myomixer expression and blocked myoblast fusion, recapitulating the phenotype upon direct genetic deletion of myomixer from zebrafish. The fusion defect in myomixer mutant embryos could be faithfully rescued upon re-expression of zebrafish myomixer gene or its orthologs from shark or human. Interestingly, myomixer mutant fish survived to adult stage though were notably smaller than wildtype siblings. Severe myopathy accompanied by the uncontrolled adipose infiltration was observed in both fast and slow muscle tissues of adult myomixer mutants. Collectively, our data highlight an indispensable role of myomixer gene for cell fusion during both embryonic muscle development and post-larval muscle growth.