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"Although in the absence of UV DAF-16::GFP was completely cytoplasmic, we observed a transient nuclear localization following UV treatment during larval stages (L1 larvae Fig. 1c; L3 larvae Supplementary Fig. 1G). DAF-16 showed nearly complete and prolonged nuclear localization in completely NER- and TC-NER-deficient mutants following UV damage, whereas GG-NER-defective worms behaved similarly to WT animals (Fig. 1c and Supplementary Fig. 1G), suggesting that transcription-blocking lesions lead to activation of DAF-16."

"Although in the absence of UV DAF-16::GFP was completely cytoplasmic, we observed a transient nuclear localization following UV treatment during larval stages (L1 larvae Fig. 1c; L3 larvae Supplementary Fig. 1G). DAF-16 showed nearly complete and prolonged nuclear localization in completely NER- and TC-NER-deficient mutants following UV damage, whereas GG-NER-defective worms behaved similarly to WT animals (Fig. 1c and Supplementary Fig. 1G), suggesting that transcription-blocking lesions lead to activation of DAF-16."

"Although in the absence of UV DAF-16::GFP was completely cytoplasmic, we observed a transient nuclear localization following UV treatment during larval stages (L1 larvae Fig. 1c; L3 larvae Supplementary Fig. 1G). DAF-16 showed nearly complete and prolonged nuclear localization in completely NER- and TC-NER-deficient mutants following UV damage, whereas GG-NER-defective worms behaved similarly to WT animals (Fig. 1c and Supplementary Fig. 1G), suggesting that transcription-blocking lesions lead to activation of DAF-16."

"Although in the absence of UV DAF-16::GFP was completely cytoplasmic, we observed a transient nuclear localization following UV treatment during larval stages (L1 larvae Fig. 1c; L3 larvae Supplementary Fig. 1G). DAF-16 showed nearly complete and prolonged nuclear localization in completely NER- and TC-NER-deficient mutants following UV damage, whereas GG-NER-defective worms behaved similarly to WT animals (Fig. 1c and Supplementary Fig. 1G), suggesting that transcription-blocking lesions lead to activation of DAF-16."

"Although in the absence of UV DAF-16::GFP was completely cytoplasmic, we observed a transient nuclear localization following UV treatment during larval stages (L1 larvae Fig. 1c; L3 larvae Supplementary Fig. 1G). DAF-16 showed nearly complete and prolonged nuclear localization in completely NER- and TC-NER-deficient mutants following UV damage, whereas GG-NER-defective worms behaved similarly to WT animals (Fig. 1c and Supplementary Fig. 1G), suggesting that transcription-blocking lesions lead to activation of DAF-16."

"Although in the absence of UV DAF-16::GFP was completely cytoplasmic, we observed a transient nuclear localization following UV treatment during larval stages (L1 larvae Fig. 1c; L3 larvae Supplementary Fig. 1G). DAF-16 showed nearly complete and prolonged nuclear localization in completely NER- and TC-NER-deficient mutants following UV damage, whereas GG-NER-defective worms behaved similarly to WT animals (Fig. 1c and Supplementary Fig. 1G), suggesting that transcription-blocking lesions lead to activation of DAF-16."

"Although in the absence of UV DAF-16::GFP was completely cytoplasmic, we observed a transient nuclear localization following UV treatment during larval stages (L1 larvae Fig. 1c; L3 larvae Supplementary Fig. 1G). DAF-16 showed nearly complete and prolonged nuclear localization in completely NER- and TC-NER-deficient mutants following UV damage, whereas GG-NER-defective worms behaved similarly to WT animals (Fig. 1c and Supplementary Fig. 1G), suggesting that transcription-blocking lesions lead to activation of DAF-16."