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鹅肥肝形成过程中脂质代谢的甲基化动态调控机制OA

Dynamic regulation mechanism of lipid metabolism methylation during the formation of goose fatty liver

中文摘要英文摘要

[目的]本研究旨在揭示DNA甲基化调控在鹅肥肝形成中的作用,以期进一步筛选和挖掘与鹅肥肝形成相关的关键代谢通路和差异甲基化基因,从而完善鹅肥肝形成的表观遗传调控机制.[方法]试验选取同批次生理状态与健康状况相同的70日龄朗德鹅,分别于填饲前期(7 d)、填饲中期(16 d)、填饲后期(25 d)随机选取3只朗德鹅进行肝脏样品采集,通过DNA甲基化组分析,进一步筛选与鹅肥肝形成相关的关键代谢通路并发掘差异甲基化基因.[结果]测序获得有效数据共266.2 G,平均Q30为87.57%,比对率约74%,CT转化效率>99.4%.在全基因组检测到的甲基化胞嘧啶中,CpG上下文类型占比约65%,甲基化水平约20%;CHG和CHH类型占比均约0.7%,甲基化水平分别约4%和1.4%.主成分分析显示各填饲阶段样本明显区分;基因功能区域中,外显子区甲基化水平最高,启动子区最低.在填饲前期与填饲中期比较组中,有524个差异甲基化区域(Differential methylated region,DMR)甲基化水平上升,427个DMR甲基化水平下降;在填饲中期与填饲后期比较组中,有432个DMR甲基化水平上升,236个DMR甲基化水平下降.前期与中期差异基因显著富集于121条KEGG通路,获得829个GO条目,其中胰岛素信号通路、FoxO信号通路等与脂质沉积密切相关,涉及MAPK10、IL6等6个基因.中期与后期差异基因富集到96条KEGG通路,获得629个GO条目,其中MAPK信号通路、FoxO信号通路等显著富集,关联基因包括MAPK10、PCK1、PLA2G4A等13个基因.[结论]DMR主要富集于脂代谢相关通路的关键基因,其形成受FoxO信号通路、脂肪细胞因子信号通路、PPAR信号通路、胰岛素信号通路等多通路的协同调控,关键候选基因MAPK10、PCK1、PLA2G4A等甲基化水平与鹅肥肝形成有关联.

[Objective]The purpose of this study was to reveal the role of DNA methylation regulation in the formation of goose fat liver,in order to further screen and explore the key metabolic pathways and differential methylation genes related to the formation of goose fat liver,so as to improve the epigenetic regulation mechanism of goose fat liver formation.[Methods]In this study,three 70-day-old Lander geese with the same physiological status and health status were selected from the same batch for liver sample collection in the early stage(7 days),middle stage(16 days)and late stage of feeding(25 days).[Results]The results showed that a total of 266.2G of valid data were obtained by sequencing,with an average Q30 of 87.57%,a match rate of about 74%,and a CT conversion efficiency of>99.4%.Among the methylated cytosine detected in the whole genome,the CpG context type accounted for about 65%and the methylation level was about 20%.CHG and CHH types accounted for about 0.7%,and the methylation levels were about 4%and 1.4%,respectively.Principal component analysis showed that the samples at each feeding stage were clearly differentiated.Among the gene function regions,the exon region had the highest methylation level and the lowest promoter region.In the comparison group in the early and middle stage of feeding,524 differential methylated region(DMR)methylation levels increased and 427 DMR methylation levels decreased.In the middle and late stage of feeding,432 DMR methylation levels increased and 236 DMR methylation levels decreased.The differential genes in the early and middle stages were significantly enriched in 121 KEGG pathways,and 829 GO entries were obtained,among which insulin signaling pathway and FoxO signaling pathway were closely related to lipid deposition,involving 6 genes such as MAPK10 and IL6.The differential genes in metaphase and late stage were enriched into 96 KEGG pathways,and 629 GO entries were obtained,among which MAPK signaling pathway and FoxO signaling pathway were significantly enriched,and 13 related genes including MAPK10,PCK1,and PLA2G4A were obtained.[Conclusion]The DMR is mainly enriched in key genes related to lipid metabolism,and its formation is synergisticly regulated by multiple pathways such as FoxO signaling pathway,adipocytokine signaling pathway,PPAR signaling pathway,insulin signaling pathway,etc.,and the methylation levels of key candidate genes MAPK10,PCK1,PLA2G4A are associated with the formation of goose fat liver.

黄鲁豫;郑赛超;王宝维;凡文磊;张名爱;岳斌;孔敏;侯中一;姜雅静;滕兴怡;刘嘉玲;赖学湘

青岛农业大学动物科技学院,山东 青岛 266109青岛农业大学动物科技学院,山东 青岛 266109青岛农业大学动物科技学院,山东 青岛 266109||青岛农业大学优质水禽研究所,山东 青岛 266109青岛农业大学动物科技学院,山东 青岛 266109||青岛农业大学优质水禽研究所,山东 青岛 266109青岛农业大学动物科技学院,山东 青岛 266109||青岛农业大学优质水禽研究所,山东 青岛 266109青岛农业大学优质水禽研究所,山东 青岛 266109青岛农业大学动物科技学院,山东 青岛 266109青岛农业大学优质水禽研究所,山东 青岛 266109青岛农业大学动物科技学院,山东 青岛 266109青岛农业大学动物科技学院,山东 青岛 266109青岛农业大学动物科技学院,山东 青岛 266109青岛农业大学食品科学与工程学院,山东 青岛 266109

农业科技

鹅肥肝甲基化脂质代谢分子机制

Goose fatty liverDNA methylationLipid metabolismMolecular mechanism

《中国畜禽种业》 2026 (7)

28-37,10

山东省重点研发计划(农业良种工程)项目(2024LZGC021)山东省自然科学基金青年项目(ZR2020QC182)国家现代农业产业技术体系(CARS-42-14).

10.19543/j.cnki.1673-4556.20260602.001

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