Yan Fang, Li Mingze, Zang Shasha, Xu Zhiguang, Bao Menglin, Wu Hongyan
School of Life Science, Ludong University, Yantai, China.
Key Laboratory of Marine Biotechnology in Universities of Shandong, Ludong University, Yantai, China.
Front Microbiol. 2024 Jan 16;15:1351796. doi: 10.3389/fmicb.2024.1351796. eCollection 2024.
The aim was to determine the response of a bloom-forming to climatic changes. Cultures of FACHB 905 were grown at two temperatures (25°C, 30°C) and exposed to high photosynthetically active radiation (PAR: 400-700 nm) alone or combined with UVR (PAR + UVR: 295-700 nm) for specified times. It was found that increased temperature enhanced sensitivity to both PAR and PAR + UVR as shown by reduced PSII quantum yields () in comparison with that at growth temperature (25°C), the presence of UVR significantly exacerbated the photoinhibition. cells grown at high temperature exhibited lower PSII repair rate () and sustained nonphotochemical quenching (NPQs) induction during the radiation exposure, particularly for PAR + UVR. Although high temperature alone or worked with UVR induced higher SOD and CAT activity and promoted the removal rate of PsbA, it seemed not enough to prevent the damage effect from them showing by the increased value of photoinactivation rate constant (). In addition, the energetic cost of microcystin synthesis at high temperature probably led to reduced materials and energy available for PsbA turnover, thus may partly account for the lower and the declination of photosynthetic activity in cells following PAR and PAR + UVR exposure. Our findings suggest that increased temperature modulates the sensitivity of to UVR by affecting the PSII repair and defense capacity, thus influencing competitiveness and abundance in the future water environment.
目的是确定一种形成水华的生物对气候变化的响应。将FACHB 905培养物在两种温度(25°C、30°C)下培养,并在特定时间单独暴露于高光量子通量密度(PAR:400 - 700 nm)或与紫外线辐射(PAR + UVR:295 - 700 nm)联合照射。结果发现,温度升高增强了对PAR和PAR + UVR的敏感性,与生长温度(25°C)相比,PSII量子产率()降低,紫外线辐射的存在显著加剧了光抑制。在高温下生长的细胞在辐射暴露期间表现出较低的PSII修复率()和持续的非光化学猝灭(NPQs)诱导,特别是对于PAR + UVR。尽管单独高温或与紫外线辐射共同作用诱导了较高的超氧化物歧化酶(SOD)和过氧化氢酶(CAT)活性,并促进了D1蛋白(PsbA)的去除率,但似乎不足以防止光失活速率常数()增加所显示的它们造成的损伤效应。此外,高温下微囊藻毒素合成的能量成本可能导致可用于D1蛋白周转的物质和能量减少,因此可能部分解释了在PAR和PAR + UVR暴露后细胞中较低的修复率和光合活性的下降。我们的研究结果表明,温度升高通过影响PSII修复和防御能力来调节该生物对紫外线辐射的敏感性,从而影响未来水环境中的竞争力和丰度。