FB2026_01 , released March 12, 2026
FB2026_01 , released March 12, 2026
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Citation
Piacenti-Silva, M., de Mattos Alves, S., Zaparoli, H.H., de Oliveira, M., Morimoto, J., Zilli Vieira, C.L. (2025). Role of visual and non-visual opsins in blue light-induced neurodegeneration in Drosophila melanogaster.  Front. Public Health 13(): 1644780.
FlyBase ID
FBrf0264149
Publication Type
Research paper
Abstract
Light plays a key role in regulating circadian rhythms and downstream physiological and behavioural functions. However, excessive exposure to artificial blue light (450-500 nm) can disrupt sleep, metabolism and neural integrity. Visual opsins mediate light-dependent signalling, but organisms also express non-visual opsins whose roles in blue-light-induced neural stress are not well understood. We used Drosophila melanogaster knockout lines lacking either visual rhodopsin 1 (Rh1[1]) or non-visual rhodopsin 7 (Rh7[1]), alongside wild-type (w[1118]) controls. Flies were continuously exposed to 488 nm blue light (1,320 lux; 1,12 μW cm[-2]) from egg deposition until they were 20 days old. DNA damage (γ-H2Av immunostaining) and vacuole formation were quantified in brain regions associated with sensory processing and neurotransmission. Rh1[1] flies exhibited the highest levels of DNA damage and vacuolisation compared to the w[1118] and Rh7[1] lines. These effects were most pronounced in neuropils linked to sensory integration and synaptic activity. Our findings demonstrate that the visual opsin Rh1 plays a predominant role in blue-light-induced DNA damage and neurodegeneration in the Drosophila central nervous system. This suggests that it is visual, rather than non-visual, opsins that mediate the neurotoxic effects of exposure to artificial light.
PubMed ID
PubMed Central ID
PMC12702751 (PMC) (EuropePMC)
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    Language of Publication
    English
    Additional Languages of Abstract
    Parent Publication
    Publication Type
    Journal
    Abbreviation
    Front. Public Health
    Title
    Frontiers in public health
    ISBN/ISSN
    2296-2565
    Data From Reference
    Alleles (2)
    Genes (2)
    Insertions (1)