UASt regulatory sequences drive expression of an inverted repeat.
Ercc1KK101553, Scer\GAL4Act88F.1.3 is an enhancer of abnormal DNA repair | adult stage phenotype of Scer\GAL4Act88F.1.3, mei-9RNAi.UAS
Ercc1KK101553, Scer\GAL4Act88F.1.3 is an enhancer of abnormal aging phenotype of Scer\GAL4Act88F.1.3, mei-9RNAi.UAS
Ercc1KK101553, Scer\GAL4Act88F.Switch.PM is a suppressor of long lived | female limited | RU486 conditional phenotype of Scer\GAL4Act88F.Switch.PM, mei-9RNAi.UAS
Ercc1KK101553, Scer\GAL4Act88F.1.3 is a suppressor of increased occurrence of cell division | adult stage | progressive phenotype of Scer\GAL4Act88F.1.3, mei-9RNAi.UAS
Ercc1KK101553, Scer\GAL4A58 is a non-suppressor of abnormal DNA repair | adult stage | conditional phenotype of Scer\GAL4A58, mei-9RNAi.UAS
Ercc1KK101553, Scer\GAL4Act88F.1.3 is an enhancer of adult somatic muscle cell of thorax phenotype of Scer\GAL4Act88F.1.3, mei-9RNAi.UAS
Ercc1KK101553, Scer\GAL4Act88F.1.3 is a suppressor of adult midgut epithelium phenotype of Scer\GAL4Act88F.1.3, mei-9RNAi.UAS
Ercc1KK101553, Scer\GAL4A58 is a non-suppressor of adult abdomen | conditional phenotype of Scer\GAL4A58, mei-9RNAi.UAS
In adults expressing mei-9dsRNA.UAS under the control of Scer\GAL4Act88F.1.3, longitudinal thoracic muscles exhibit DNA damage (phospho-H2AvD staining) and premature aging (progressive loss of proteostasis); both of these are robustly enhanced by the co-expression of Ercc1KK101553, which is highlighted by a premature loss of proteostasis and disruption of myofibril muscle structure during aging. 30-days adults expressing mei-9dsRNA.UAS also present increased mitosis in the midgut, which is also suppressed by the co-expression of Ercc1KK101553.
The UV-induced cuticle defects observed in the abdomen of adults expressing mei-9dsRNA.UAS under the control of Scer\GAL4A58 are not suppressed by the co-expression of Ercc1KK101553.