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REPOSITORIES: ENA
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Project description:Mandarin fish Siniperca chuatsi (Basilewsky) (Percichthyidae), as a demersal piscivore, has very specialized feeding habits, for as soon as they start feeding the fry of this fish feed solely on fry of other fish species. In rearing conditions, mandarin fish has been found to accept live prey fish only, and refuse dead prey fish or artificial diets, very little is currently known about the molecular mechanisms of multiple genes which cover different pathways influencing the specialized food habit, such as live prey. We performed transcriptome comparisons between dead prey fish feeders and nonfeeders in mandarin fish. The determination mechanisms of specialized food habit (live prey fish) in mandarin fish could provide some instructions for research of food habit in animals, including mammals.
2013-10-21 | E-MTAB-1365 | biostudies-arrayexpress
Project description:The determination mechanisms of specialized food habit (live prey fish) in mandarin fish
| PRJEB631 | ENA
Project description:To characterize the site-specific methylation landscape of the Mandarin fish ranavirus (MRV) genome, whole-genome bisulfite sequencing (WGBS) was conducted on an isolated MRV strain.
2024-04-02 | GSE262554 | GEO
Project description:Venomous animals have evolved diverse molecular mechanisms to incapacitate prey and defend against predators. The majority of venom components characterized to date disrupt the nervous, locomotor, and cardiovascular system or causes tissue damage and degradation. The discovery that certain species of fish-hunting cone snail use weaponized insulins to induce hypoglycemic shock in prey provided an unusual example for the use of toxins that target glucose homeostasis. Here, we show that, in addition to insulins, the deadly fish hunter, Conus geographus, uses a selective agonist of the somatostatin receptor 2 (SSTR2) that potently blocks the release of the insulin-counteracting hormone glucagon, thereby exacerbating insulin-induced hypoglycemia in prey. The native toxin, Consomatin nG1, exists in several proteoforms that contain a minimized vertebrate somatostatin-like core motif connected to a heavily glycosylated N-terminal region. We demonstrate that the toxin’s N-terminal tail aligns with a glycosylated somatostatin peptide previously identified from fish pancreas and plays an important role in activating the fish SSTR2. Collectively, these findings provide a stunning example of chemical mimicry, highlight the combinatorial nature of venom components, and establish glucose homeostasis as an effective target for prey capture.
2024-06-26 | PXD052869 | Pride
Project description:Venomous animals have evolved diverse molecular mechanisms to incapacitate prey and defend against predators. The majority of venom components characterized to date disrupt the nervous, locomotor, and cardiovascular system or causes tissue damage and degradation1. The discovery that certain species of fish-hunting cone snail use weaponized insulins to induce hypoglycemic shock in prey provided an unusual example for the use of toxins that target glucose homeostasis2. Here, we show that, in addition to insulins, the deadly fish hunter, Conus geographus, uses a selective agonist of the somatostatin receptor 2 (SSTR2) that potently blocks the release of the insulin-counteracting hormone glucagon, thereby exacerbating insulin-induced hypoglycemia in prey. The native toxin, Consomatin nG1, exists in several proteoforms that contain a minimized vertebrate somatostatin-like core motif connected to a heavily glycosylated N-terminal region. We demonstrate that the toxin’s N-terminal tail aligns with a glycosylated somatostatin peptide previously identified from fish pancreas and plays an important role in activating the fish SSTR2. Collectively, these findings provide a stunning example of chemical mimicry, highlight the combinatorial nature of venom components, and establish glucose homeostasis as an effective target for prey capture.
2024-06-26 | PXD053107 | Pride