AI Article Synopsis
- The study focused on how tilapia brain cells respond genetically to hypertonic stress, identifying a total of 331 known and 163 novel miRNAs involved in this response.
- It found that 16 miRNAs were significantly upregulated and 11 downregulated, affecting key processes like metabolism, immune response, and neural regulation, with implications for neurotrophic and synaptic signaling pathways.
- The research highlights the importance of miRNA expression changes in regulating osmotic pressure, providing a foundation for further study on miRNA functions and potentially aiding aquaculture practices in harsh water conditions.
Article Abstract
This study investigated the genetic response of tilapia (Oreochromis mossambicus) brain cells to hypertonic stress, focusing on miRNAs regulation. Three hundred and thirty-one known miRNAs and 163 novel miRNAs which responded to hypertonic stress were identified by high-throughput sequencing in tilapia brain cells. Differential expression analysis revealed that 16 miRNAs were significantly upregulated, while 11 miRNAs were significantly downregulated. These differentially expressed miRNAs are closely related to metabolism, immune response, and neural regulation. The target genes of these miRNAs are implicated in neurotrophic and synaptic signaling pathways, potentially affecting metabolic and apoptotic processes. GO and KEGG enrichment analyses provided insights into the biological processes and pathways affected by hypertonic stress. Furthermore, correlation analysis between mRNA and miRNA highlighted miRNA-mRNA interactions related to cell cycle and apoptosis regulation. These results indicated significant changes of miRNA expression under hypertonic stress and their crucial role in osmotic pressure regulation. This study offers a basis for further exploration of miRNA functions and molecular mechanisms in tilapia, potentially informing practices for aquaculture in challenging environments such as saline-alkaline waters.
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| http://dx.doi.org/10.1016/j.cbd.2024.101350 | DOI Listing |
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