Additional file 1 of Simple model systems reveal conserved mechanisms of Alzheimer’s disease and related tauopathies

Additional file 1: Table S1. Genetic modifiers of AD identified in S. cerevisiae models. Table S2. Genetic modifiers of AD identified in C. elegans models. Table S3. Genetic modifiers of AD identified in Drosophila models. Table S4. Human orthologs of genetic modifiers identified in Aβ models. Human orthologs of S. cerevisiae genes were retrieved from the Saccharomyces Genome Database (SGD) YeastMine online tool. Orthologs of C. elegans genes were queried from the OrthoList2 online tool. Orthologs of Drosophila genes were obtained from FlyBase. AD genes identified from GWAS studies are highlighted in red. Table S5. Human orthologs of genetic modifiers identified in Tau models. Orthologs of S. cerevisiae genes were retrieved from the SGD YeastMine online tool. Orthologs of C. elegans genes were queried from the OrthoList2 online tool. Orthologs of Drosophila genes were obtained from FlyBase. AD genes identified from GWAS studies are highlighted in red. Table S6. Functional classes enrichment of Aβ modifiers identified in S. cerevisiae models analyzed using FunSpec. Gene list was queried to multiple yeast databases including GO Molecular Function, GO Biological Process, GO Cellular Component, MIPS Functional Classification, MIPS Phenotypes, MIPS Subcellular Localization, MIPS Protein Complexes using FunSpec. Table S7. Cellular pathways and processes linked to Tau modifiers. GO analysis of Tau modifiers identified in S. cerevisiae models was performed using FunSpec. Tau modifiers identified in C.elegansmodels were analyzed using the WormCat online tool. Tau modifiers identified in Drosophila models were grouped using the GLAD database. Table S8. Functional annotation and enrichment of Aβ modifiers identified in C. elegans models analyzed using WormCat. Gene list were input to WormCat using default settings for analyzation. Promoting genes indicated that deletion/reduction suppresses AD phenotypes and/or overexpression enhances AD phenotypes. Preventing genes indicated that deletion/reduction enhances AD phenotypes and/or overexpression suppresses AD phenotypes. Table S9. Functional annotation and enrichment of Tau modifiers identified in C. elegans models analyzed using WormCat. Gene lists were analyzed using WormCat. Promoting genes indicated that deletion/reduction suppresses AD phenotypes and/or overexpression enhances AD phenotypes. Preventing genes indicated that deletion/reduction enhances AD phenotypes and/or overexpression suppresses AD phenotypes. Table S10. Functional classes enrichment of Aβ modifiers identified in S. cerevisiae models analyzed using GO Slim Mapper. Gene list was queried to SGD Yeast GO-Slim database. Table S11. Functional annotation and enrichment of Aβ modifiers identified in C. elegans models analyzed using WormCat. Gene list were input to WormCat using default settings for analyzation. Promoting genes indicated that deletion/reduction suppresses AD phenotypes and/or overexpression enhances AD phenotypes. Preventing genes indicated that deletion/reduction enhances AD phenotypes and/or overexpression suppresses AD phenotypes. Table S12. Functional annotation and enrichment of Aβ modifiers identified in Drosophila models analyzed using GLAD. Gene list was analyzed using Find Group Membership function in the GLAD online tool [5, 6, 12, 19, 26, 28, 31, 33, 38, 39, 44, 47, 48, 52, 56, 57, 61, 68, 71, 73–75, 77, 79, 85, 90, 95–98, 100, 102, 111, 113, 115, 121, 131, 137, 145, 146, 152, 153, 155, 157, 161, 163, 164, 166, 170, 174, 175, 177–179, 181, 186, 188, 190, 192, 197, 199, 200, 202, 203, 211, 217–219, 223, 228, 230, 231, 237, 239, 241, 244, 246, 247, 253, 259, 262, 265, 272, 273, 280, 290, 292, 293, 295, 296, 298, 303, 306, 307, 310, 315, 316, 318, 319, 323, 326, 332–334, 336, 337].

附加文件1：表S1。酿酒酵母（S. cerevisiae）模型中鉴定出的阿尔茨海默病（Alzheimer's disease，AD）遗传修饰因子。表S2：秀丽隐杆线虫（C. elegans）模型中鉴定出的AD遗传修饰因子。表S3：果蝇（Drosophila）模型中鉴定出的AD遗传修饰因子。表S4：淀粉样β蛋白（Aβ）模型中鉴定出的遗传修饰因子的人类同源基因。酿酒酵母基因的人类同源基因从酿酒酵母基因组数据库（Saccharomyces Genome Database，SGD）YeastMine在线工具获取；秀丽隐杆线虫基因的同源基因从OrthoList2在线工具查询；果蝇基因的同源基因从FlyBase获取。全基因组关联研究（Genome-Wide Association Study，GWAS）鉴定出的AD基因以红色标注。表S5：Tau蛋白模型中鉴定出的遗传修饰因子的人类同源基因。酿酒酵母基因的人类同源基因从SGD YeastMine在线工具获取；秀丽隐杆线虫基因的同源基因从OrthoList2在线工具查询；果蝇基因的同源基因从FlyBase获取。GWAS鉴定出的AD基因以红色标注。表S6：利用FunSpec工具对酿酒酵母模型中鉴定出的Aβ修饰因子进行功能类别富集分析。将基因列表提交至多个酵母数据库进行分析，包括GO分子功能、GO生物过程、GO细胞组分、慕尼黑蛋白质序列信息中心（MIPS）功能分类、MIPS表型、MIPS亚细胞定位、MIPS蛋白质复合物。表S7：与Tau蛋白修饰因子相关的细胞通路与过程。利用FunSpec工具对酿酒酵母模型中鉴定出的Tau修饰因子进行GO富集分析；利用WormCat在线工具对秀丽隐杆线虫模型中鉴定出的Tau修饰因子进行分析；利用GLAD数据库对果蝇模型中鉴定出的Tau修饰因子进行分组。表S8：利用WormCat工具对秀丽隐杆线虫模型中鉴定出的Aβ修饰因子进行功能注释与富集分析。将基因列表以默认参数输入WormCat进行分析。促病变基因指其缺失/表达下调可抑制AD表型，或过表达可增强AD表型；抑病变基因指其缺失/表达下调可增强AD表型，或过表达可抑制AD表型。表S9：利用WormCat工具对秀丽隐杆线虫模型中鉴定出的Tau修饰因子进行功能注释与富集分析。利用WormCat工具对基因列表进行分析。促病变基因指其缺失/表达下调可抑制AD表型，或过表达可增强AD表型；抑病变基因指其缺失/表达下调可增强AD表型，或过表达可抑制AD表型。表S10：利用GO Slim Mapper工具对酿酒酵母模型中鉴定出的Aβ修饰因子进行功能类别富集分析。将基因列表提交至SGD酵母GO-Slim数据库。表S11：利用WormCat工具对秀丽隐杆线虫模型中鉴定出的Aβ修饰因子进行功能注释与富集分析。将基因列表以默认参数输入WormCat进行分析。促病变基因指其缺失/表达下调可抑制AD表型，或过表达可增强AD表型；抑病变基因指其缺失/表达下调可增强AD表型，或过表达可抑制AD表型。表S12：利用GLAD工具对果蝇模型中鉴定出的Aβ修饰因子进行功能注释与富集分析。利用GLAD在线工具中的“查找组成员”功能对基因列表进行分析。参考文献[5, 6, 12, 19, 26, 28, 31, 33, 38, 39, 44, 47, 48, 52, 56, 57, 61, 68, 71, 73–75, 77, 79, 85, 90, 95–98, 100, 102, 111, 113, 115, 121, 131, 137, 145, 146, 152, 153, 155, 157, 161, 163, 164, 166, 170, 174, 175, 177–179, 181, 186, 188, 190, 192, 197, 199, 200, 202, 203, 211, 217–219, 223, 228, 230, 231, 237, 239, 241, 244, 246, 247, 253, 259, 262, 265, 272, 273, 280, 290, 292, 293, 295, 296, 298, 303, 306, 307, 310, 315, 316, 318, 319, 323, 326, 332–334, 336, 337]