BAZ-2和SET-6通过BLMP-1调控秀丽隐杆线虫衰老

该文使用秀丽隐杆线虫作为模式动物, 探讨了两个表观遗传因子BAZ-2和SET-6通过 BLMP-1调控编码线粒体功能蛋白核基因的表达, 进而调控线虫衰老。利用JASPAR数据库, 分析了baz-2和set-6突变体线虫中表达上调基因的启动子区域DNA序列, 发现转录因子BLMP-1的特征结合位点在这些序列中富集。随后分别在baz-2和set-6突变体线虫中敲除blmp-1基因, 检测blmp1;baz-2和blmp-1;set-6双敲除突变体线虫的寿命、咽喉肌肉跳动能力、基础型和增强型食物诱导的缓慢运动反应、抗氧化应激能力和线粒体功能相关基因的表达水平, 发现敲除blmp-1消除了baz-2 和set-6突变体线虫寿命较长, 咽喉肌肉跳动、基础型和增强型食物诱导的缓慢运动反应和抗氧化能力较好的行为表型, 以及线粒体功能相关基因表达上调的现象。该研究阐明了BAZ-2和SET-6通过BLMP-1调控线虫衰老的机制。

This study used Caenorhabditis elegans as a model organism to investigate that two epigenetic factors, BAZ-2 and SET-6, regulate the expression of nuclear genes encoding mitochondrial functional proteins via BLMP-1, thereby modulating nematode aging. Using the JASPAR database, we analyzed the promoter region DNA sequences of upregulated genes in baz-2 and set-6 mutant nematodes, and found that the characteristic binding sites of transcription factor BLMP-1 were enriched in these sequences. Subsequently, we knocked out the blmp-1 gene in baz-2 and set-6 mutant nematodes respectively, and examined the lifespan, pharyngeal muscle pumping rate, basal and enhanced food-induced slowing responses, oxidative stress resistance, and expression levels of mitochondrial function-related genes in blmp-1;baz-2 and blmp-1;set-6 double knockout mutant nematodes. We found that knocking out blmp-1 abolished the favorable behavioral phenotypes including longer lifespan, improved pharyngeal muscle pumping, basal and enhanced food-induced slowing responses, and enhanced oxidative stress resistance, as well as the upregulated expression of mitochondrial function-related genes in baz-2 and set-6 mutant nematodes. This study elucidated the mechanism by which BAZ-2 and SET-6 regulate nematode aging via BLMP-1.

搜集汇总

背景与挑战

背景概述

该数据集聚焦于秀丽隐杆线虫衰老机制研究，探索表观遗传调节因子BAZ-2和SET-6如何通过转录因子BLMP-1调控线粒体相关核基因表达，从而影响寿命和行为。实验数据表明，blmp-1的缺失会消除baz-2或set-6突变体带来的寿命延长效应，揭示了BLMP-1在衰老调控中的关键作用。数据集由中国科学院脑科学与智能技术卓越中心于2024年发布，包含原始实验数据，适用于衰老生物学和基因调控网络研究。