Additional file 1: of Mitochondrial unfolded protein response transcription factor ATFS-1 promotes longevity in a long-lived mitochondrial mutant through activation of stress response pathways
Creators: name: Ziyun Wu
name: Senchuk, Megan
name: Dues, Dylan
name: Johnson, Benjamin
name: Cooper, Jason
name: Leira Lew
name: Machiela, Emily
name: Schaar, Claire
name: DeJonge, Heather
name: T. Blackwell
name: Raamsdonk, Jeremy Van
Publisher: name: figshare
Year: 2018
Subjects: subject: Biochemistry
subject: Medicine
subject: Microbiology
subject: FOS: Biological sciences
subject: FOS: Biological sciences
subject: Genetics
subject: Molecular Biology
subject: Physiology
subject: Immunology
subject: FOS: Clinical medicine
subject: FOS: Clinical medicine
subject: Developmental Biology
subject: Cancer
subject: 110309 Infectious Diseases
subject: FOS: Health sciences
subject: FOS: Health sciences
subject: Plant Biology
subject: Computational Biology

description: Figure S1. hsp-6 mRNA levels are increased in young adult clk-1, isp-1 and nuo-6 worms and correlated with atfs-1 mRNA levels. Figure S2. Activation of the mitochondrial unfolded protein response in long-lived mitochondrial mutants is dependent on atfs-1. Figure S3. Treatment with antioxidants does not prevent activation of the mitochondrial unfolded protein response in nuo-6 mutants. Figure S5. ATFS-1 is required for development to adulthood in clk-1 and isp-1 worms. Figure S6. nuo-6 worms requires UBL-5 and DVE-1 to develop to adulthood. Figure S7. haf-1 is not required for the longevity of the long-lived mitochondrial mutant nuo-6. Figure S8. Effect of knocking down components of the mitochondrial unfolded protein response on activation of the cytoplasmic unfolded protein response. Figure S9. Mitochondrial unfolded protein response is activated in sod-2 mutants but not required for their longevity. Figure S10. Restoring atfs-1 expression during adulthood reverts lifespan to nuo-6. Figure S11. Disruption of atfs-1 decreases levels of reactive oxygen species (ROS). Figure S12. Activation of cytosolic unfolded protein response in atfs-1 mutants is HSF-1-dependent and DAF-16-independent. Figure S13. ATFS-1 is required for the activation of stress response pathways in nuo-6 worms. Figure S14. The expression of antioxidant defense genes is not significantly modulated by atfs-1 deletion. Figure S15. HIF-1-regulated gene expression changes in nuo-6 mitochondrial mutant. Figure S16. Reactome enrichment for genes upregulated in nuo-6 mutants and reverted to wild-type in nuo-6;hif-1 double mutants. Figure S17. Reactome enrichment for genes downregulated altered in nuo-6 mutants and reverted to wild-type in nuo-6;hif-1 double mutants. Figure S18. Loss of atfs-1 decreases nuclear localization of DAF-16. Figure S19. ATFS-1-regulated gene expression changes in nuo-6 mitochondrial mutant. Figure S20. Reactome enrichment for genes upregulated in nuo-6 mutants and reverted to wild-type in nuo-6;atfs-1 double mutants. Figure S21. Reactome enrichment for genes downregulated in nuo-6 mutants and reverted to wild-type in nuo-6;atfs-1 double mutants. Figure S22. atfs-1 gain-of-function mutants show a highly significant overlap in gene expression changes with clk-1 mutants. Figure 23. atfs‐1 gain‐of‐function mutants show a highly significant overlap in gene expression changes with isp‐1 mutants. Table S1. atfs‐1 gain‐of‐function mutants exhibit statistically significant overlap in gene expression changes with daf‐2 mutants. (PDF 2446 kb)