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微藻小球藻的细胞周期被神经毒素 β-N-甲基氨基-l-丙氨酸阻断及相应的分子机制。

Cell cycle of microalga Isochrysis galbana arrested by neurotoxin β-N-methylamino-l-alanine and corresponding molecular mechanisms.

机构信息

College of Environmental Science and Engineering, Ocean University of China, Qingdao 266100, China; Key Laboratory of Marine Environment and Ecology, Ocean University of China, Ministry of Education, Qingdao 266100, China.

College of Environmental Science and Engineering, Ocean University of China, Qingdao 266100, China.

出版信息

Sci Total Environ. 2023 May 20;874:162445. doi: 10.1016/j.scitotenv.2023.162445. Epub 2023 Feb 26.

DOI:10.1016/j.scitotenv.2023.162445
PMID:36848993
Abstract

The phycotoxin β-N-methylamino-l-alanine (BMAA) has attracted attention due to its risks to marine organisms and human health. In this study, approximately 85 % of synchronized cells of the marine microalga Isochrysis galbana were arrested at the cell cycle G1 phase by BMAA at 6.5 μM for a 24-h exposure. The concentration of chlorophyll a (Chl a) gradually decreased, while the maximum quantum yield of PSII (F/F), the maximum relative electron transport rate (rETR), light utilization efficiency (α) and half-saturated light irradiance (I) reduced early and recovered gradually in I. galbana exposed to BMAA in 96-h batch cultures. Transcriptional expression of I. galbana analyzed at 10, 12, and 16 h disclosed multiple mechanisms of BMAA to suppress the microalgal growth. Production of ammonia and glutamate was limited by the down-regulation of nitrate transporters, glutamate synthase, glutamine synthetase, cyanate hydrolase, and formamidase. Diverse extrinsic proteins related to PSII, PSI, cytochrome b6f complex, and ATPase were influenced by BMAA at transcriptional level. Suppression of the DNA replication and mismatch repair pathways increased the accumulation of misfolded proteins, which was reflected by the up-regulated expression of proteasome to accelerate proteolysis. This study improves our understanding of the chemical ecology impacts of BMAA in marine ecosystems.

摘要

海洋微藻塔玛亚历山大藻细胞周期同步化及β-N-甲基氨基-L-丙氨酸(BMAA)对其的毒性效应

β-N-甲基氨基-L-丙氨酸(BMAA)因其对海洋生物和人类健康的危害而受到关注。在这项研究中,6.5 μM 的 BMAA 使约 85%的同步化塔玛亚历山大藻细胞在细胞周期 G1 期被阻滞,暴露 24 小时。叶绿素 a(Chl a)浓度逐渐降低,而 PSII 的最大光化学量子产量(F/F)、最大相对电子传递速率(rETR)、光能利用效率(α)和半饱和光强(I)在暴露于 BMAA 的塔玛亚历山大藻 96 小时分批培养中早期降低,随后逐渐恢复。在 10、12 和 16 小时分析塔玛亚历山大藻的转录表达,揭示了 BMAA 抑制微藻生长的多种机制。硝酸盐转运蛋白、谷氨酸合酶、谷氨酰胺合成酶、氰胺水解酶和脒基水解酶的下调限制了氨和谷氨酸的产生。与 PSII、PSI、细胞色素 b6f 复合物和 ATP 酶相关的多种外在蛋白在转录水平上受到 BMAA 的影响。DNA 复制和错配修复途径的抑制增加了错误折叠蛋白的积累,这反映在蛋白酶体的上调表达以加速蛋白水解上。本研究提高了我们对海洋生态系统中 BMAA 的化学生态学影响的认识。

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