类固醇激素在达里湖瓦氏雅罗鱼渗透压调节机制中的作用OA北大核心CSTPCD
Role of steroid hormones in osmoregulation mechanism of Leuciscus waleckii in Dali Lake
为探究类固醇激素在达里湖瓦氏雅罗鱼(Leuciscus waleckii)渗透压调节机制中的作用,本研究设置为期10 d的50 mmol/L NaHCO3碱胁迫和淡水恢复双向跨境胁迫实验,对不同处理组的血清类固醇激素含量及鳃组织相关基因表达量进行了关联分析,并对关键基因启动子区进行了甲基化鉴定.结果发现:不同处理组差异类固醇激素主要富集在3个通路.在类固醇生物合成通路,胆固醇含量和参与其合成途径的关键基因(hisd17b7、ebp、dhcr24、dhcr7)表达量在碱胁迫组显著升高(P<0.05),在淡水恢复组极显著降低(P<0.01);在初级胆汁酸生物合成通路,25-羟基胆固醇和7α,25-二羟基胆固醇含量及其靶基因(ch25h、cyp7a1)表达量在碱胁迫组极显著升高,在淡水恢复组极显著降低(P<0.01);在类固醇激素生物合成通路,孕烯醇酮、17α-羟孕酮、脱氧可的松和皮质醇含量在碱胁迫组极显著降低(P<0.001),在淡水恢复组显著升高(P<0.05).其中,胆固醇是这3个通路共享的中间产物.另外,合成胆固醇的关键基因ebp和催化其分解代谢的关键基因sult2b1的启动子区受甲基化修饰,且均在碱胁迫组呈低甲基化水平,在淡水恢复组呈高甲基化水平.上述研究表明,胆固醇是类固醇激素相关通路的关键产物,通过改变其合成和代谢关键基因启动子甲基化水平,调控通路上其他关键基因在不同环境下差异表达,影响类固醇激素含量,参与达里湖瓦氏雅罗鱼在不同环境的渗透压调节.
The Amur ide(Leuciscus waleckii)in Lake Dali exhibits remarkable salt-alkali resistance,thriving in environments with an alkalinity of 53.57 mmol/L and pH of 9.6.It also demonstrates reproductive migration behavior,migrating annually to freshwater rivers to spawn.During this migration,the fish must face the transition of high-permeability to low-permeability water,which involves immense energy redistribution for basic metabolism and gonadal development.Steroid hormones,which are lipid hormones synthesized from cholesterol through a series of enzymatic reactions,play a crucial role in osmoregulation,gonadal development,and energy consumption during fish reproductive migration.To explore the role of steroid hormones in the osmoregulatory pressure mechanism of Leuciscus waleckii,we conducted a 10 d bidirectional cross-border stress experiment involving 50 mmol/L NaHCO3 alkalinity stress followed by freshwater recovery.We analyzed serum steroid hormone levels,gene expression related to gill tissue in different treatment groups,and examined the methylation of key genes in promoter regions.Our results showed that differences in steroid hormones were primarily associated with three pathways.In the steroid biosynthesis pathway,the cholesterol and key genes involved(hsd17b7,ebp,dhcr24,and dhcr7)significantly increased in the alkalinity stress group(P<0.05)and significantly decreased in the freshwater recovery group(P<0.01).In the primary bile acid biosynthesis pathway,25-hydroxycholesterol and 7α,25-hydroxycholesterol,along with their target genes(ch25h and cyp7a1),significantly increased in the alkalinity stress group and significantly decreased in the freshwater recovery group(P<0.01).In the steroid hormone biosynthesis pathway,Pregnenolone,17α-hydroxyprogesterone,cortexolone,and cortisol significantly reduced in the alkalinity stress group(P<0.001)and significantly increased in the freshwater recovery group(P<0.05).Cholesterol,an intermediate product shared by these three pathways,also showed notable changes.Additionally,the promoter regions of the key genes involved in cholesterol synthesis and metabolism,ebp and sult2b1,exhibited low methylation levels in the alkalinity stress group and high methylation levels in the freshwater recovery group.These findings suggest that cholesterol is a crucial component of the steroid hormone-related pathways.It influences the methylation levels of key gene promoter regions involved in its synthesis and metabolism,thereby regulating the differential expression of other key genes in response to different environmental conditions.This regulation impacts the content of steroid hormones and plays a role in the osmoregulation of Leuciscus waleckii in varying environments.The results of this study provide a theoretical basis and scientific guidance for understanding the molecular mechanisms of fish alkali resistance,as well as for the transplantation and domestication of fish,and the cultivation of novel alkali-resistant varieties.
李雯;黄晶;邹宇婷;张立民;常玉梅
中国水产科学研究院黑龙江水产研究所,淡水鱼类育种国家地方联合工程实验室,黑龙江哈尔滨 150070||上海海洋大学水产与生命学院,上海 201306中国水产科学研究院黑龙江水产研究所,淡水鱼类育种国家地方联合工程实验室,黑龙江哈尔滨 150070
水产学
瓦氏雅罗鱼类固醇激素渗透压调节甲基化盐碱水
Leuciscus waleckiisteroid hormoneosmoregulationmethylationsaline alkali water
《中国水产科学》 2024 (008)
867-882 / 16
国家自然科学基金项目(32273120);中国水产科学研究院中央级公益性科研院所基本科研业务费专项(2023TD22).
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