Lack of Blm Helicase, but Not Hydroxyurea-Induced DNA Damage, Alters Circadian Period in Drosophila melanogaster
Faculty Mentor Information
Dr. Eric Stoffregen, Lewis-Clark State College
Presentation Date
7-15-2026
Abstract
Bloom syndrome in humans, caused by mutations in the BLM DNA helicase, is characterized by genomic instability and sensitivity to replication stress, and molecular links between DNA damage response pathways and the circadian clock have been reported across organisms. We previously observed that progeny of Drosophila Blm mutant mothers exhibit sleep and circadian abnormalities. Here we test whether Blm deficiency and hydroxyurea induced developmental DNA damage affect adult circadian and sleep behavior, using Blm null mutants and heterozygous controls monitored by the Drosophila Activity Monitor (DAM2). Hydroxyurea caused differential survival, with mutants surviving at roughly two-thirds the heterozygote rate, confirming Blm-relevant damage rather than generic toxicity. In surviving adults, hydroxyurea produced no robust circadian disruption and no reproducible genotype × treatment interactions. Blm genotype alone had pronounced effects: in constant darkness, mutants showed a longer free-running period and male mutants were hyperactive, independent of treatment. These findings link Blm genotype to circadian behavior beyond the previously observed maternal effect. Because hydroxyurea selectively killed mutants, the absent treatment effect may reflect survivor selection, pre-existing DNA damage in the mutants, or damage that kills dividing cells while sparing those that control circadian function.
Lack of Blm Helicase, but Not Hydroxyurea-Induced DNA Damage, Alters Circadian Period in Drosophila melanogaster
Bloom syndrome in humans, caused by mutations in the BLM DNA helicase, is characterized by genomic instability and sensitivity to replication stress, and molecular links between DNA damage response pathways and the circadian clock have been reported across organisms. We previously observed that progeny of Drosophila Blm mutant mothers exhibit sleep and circadian abnormalities. Here we test whether Blm deficiency and hydroxyurea induced developmental DNA damage affect adult circadian and sleep behavior, using Blm null mutants and heterozygous controls monitored by the Drosophila Activity Monitor (DAM2). Hydroxyurea caused differential survival, with mutants surviving at roughly two-thirds the heterozygote rate, confirming Blm-relevant damage rather than generic toxicity. In surviving adults, hydroxyurea produced no robust circadian disruption and no reproducible genotype × treatment interactions. Blm genotype alone had pronounced effects: in constant darkness, mutants showed a longer free-running period and male mutants were hyperactive, independent of treatment. These findings link Blm genotype to circadian behavior beyond the previously observed maternal effect. Because hydroxyurea selectively killed mutants, the absent treatment effect may reflect survivor selection, pre-existing DNA damage in the mutants, or damage that kills dividing cells while sparing those that control circadian function.