Abstract
In the present study, we showed that in the retina of Drosophila, the expression of the ho gene, encoding haeme oxygenase (HO), is regulated by light but only at the beginning of the day. This timing must be set by the circadian clock as light pulses applied at other time points during the day do not increase the ho mRNA level. Moreover, light-induced activation of HO does not depend on the canonical phototransduction pathway but instead involves cryptochrome and is enhanced by ultraviolet (UV) light. Interestingly, the level of DNA damage in the retina after UV exposure was inversely related to the circadian oscillation of the ho mRNA level during the night, being the highest when the HO level was low and reversed during the day. Accordingly, induction of HO by hemin was associated with low DNA damage, while inhibition of HO activity by SnPPIX aggravated the damage. Our data suggest that HO acts in the retina to decrease oxidative DNA damage in photoreceptors caused by UV-rich light in the morning.
Highlights
Haeme oxygenase (HO) catalyses the degradation of haeme to carbon monoxide (CO), ferrous ions and biliverdin
We found that ho expression was highest in the morning in the light/dark cycle (LD 12:12, 12 h of light and 12 h of darkness) and after a 1-h light pulse at CT1 (1 h after the beginning of the subjective day) in constant darkness (DD) (Fig. 1)
Blue light was effective at a 25–60 lx intensity, but red, green or white light without UV did not change the level of ho mRNA (Fig. 3)
Summary
Milena Damulewicz[1], Agnieszka Loboda[2], Alicja Jozkowicz[2], Jozef Dulak2 & Elzbieta Pyza[1]. At the end of the night, the amount of these gene products is sufficient to form PERIOD (PER) and TIMELESS (TIM) heterodimers[7], and PER/TIM complexes are transported into the nucleus, where they bind to CLK/CYC and repress their activity, thereby inhibiting the transcription of their own genes per and tim[8] This is the main negative feedback loop of the molecular circadian clock. PLC is a key protein in the phototransduction cascade; the norpA mutant shows a weak response to light[19, 20] This indicates that the classical rhodopsin-dependent phototransduction pathway is not the only one active in the retinal photoreceptors of D. melanogaster. We examined whether HO protects photoreceptors against UV-dependent degeneration
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