Objective: Our research aims to investigate the specific mechanisms by which copper inhibits the asexual proliferation of Aurelia coerulea polyps. Methods: Aurelia coerulea polyps were exposed to various CuSO4 concentrations to study metamorphosis and budding proliferation. Oxidative stress markers (ROS, MDA, CAT, H2O2, T-AOC, SOD) were measured in polyps and early strobilae. Transcriptomic analysis were used to compare differences in gene expression and enrichment pathways between untreated and copper-exposed polyps. Additionally, RT-qPCR was used to analyze the expression of key molecules. Antioxidant L-Ascorbic acid was applied to determine the role of oxidative stress in asexual reproduction of Aurelia coerulea polyps when exposed to copper. Results: Copper inhibited strobilization and budding of Aurelia coerulea polyps in a dose-dependent manner, in which oxidative stress was involved. Transcriptomic data suggested that the DNA replication pathway was significantly enriched in early strobilae compared to polyps. However, copper treatment repealed the difference of DNA replication pathway between early strobilae compared and polyps. Transcriptomic data suggested that alanine, aspartate, and glutamate metabolism pathways were enriched in untreated budding polyps compared to copper-exposed polyps. After applying the antioxidant L-Ascorbic acid to copper-exposed polyps, various oxidative indicators changed to different extents, with increases in ROS, MDA, CAT, H2O2, and SOD and a decrease in T-AOC. Further more, the time required for polyps to develop into early strobila was shortened, indicating that the delay in metamorphosis caused by copper exposure was effectively alleviated. And the budding rate increased, indicating that the inhibition of budding proliferation caused by copper exposure was effectively alleviated. The expression of key genes were consist with the transcriptomic sequencing results. Conclusion: Copper exposure causes oxidative stress resulting in the inhibition of asexual reproduction in Aurelia coerulea polyps, including metamorphosis and budding.

Introduction: The modification of the marine ecological environment has led to the frequent occurrence of jellyfish blooms, causing global hazards. The budding reproduction of jellyfish polyps is a critical factor in their population size, yet there is limited understanding of the molecular mechanisms involved in this process. This study aims to explore the intrinsic regulatory factors of the budding of jellyfish Aurelia coerulea (A. coerulea) polyps from the perspective of jellyfish biotoxin and to develop new strategies for the management of jellyfish abundance.Methods: The main biological toxins of the A. coerulea polyp were screened through the integrated analysis of transcriptomic and proteomic data. The broad-spectrum metalloproteinase inhibitor, ethylenediaminetetraacetic acid (EDTA), was employed to treat polyps for observing its effect on the budding of A. coerulea polyps. Through conducting the detection of metzincin proteolytic activity, molecular docking and kinetic analysis, as well as transcriptomic analysis and RT-qPCR verification before and after EDTA treatment of the polyp, the key biological toxins and the mechanisms influencing polyp budding were clarified.Results: Four types of the metzincin family of metalloproteinases constituted the main biotoxins in the A. coerulea polyp. Among them, astacins (NAS) were the predominant metzincins of the A. coerulea polyp. We discovered that EDTA significantly inhibited the activity of metzincins and the budding of A. coerulea polyps. EDTA was capable of stably binding to the zinc-binding active sites of the four major types of metzincins in the A. coerulea polyp and could down-regulate the expression levels of key metzincin molecules and enrich multiple pathways related to development.Conclusion: This study elucidates the effects of metzincins on the budding of jellyfish polyps, providing a potential target for mitigating jellyfish blooms.