Regulation Of Light Sensation By Antioxidants And Hydrogen Peroxide In C.elegans

The ability to sense and react to environmental stimuli is essential for animal survival.One of the most common stimuli is light.The nematode Caenorhabditis elegans is a model organism widely used in laboratory.C.elegans has long been believed to lack the ability to sense light due to the absence of photoreceptor system and its original isolation in soil samples.Recently,researchers revealed that C.elegans exhibits robust phototaxis behavior in response to short-wavelength light,particularly UV light.C.elegans senses light through LITE-1,a unique photoreceptor protein that belongs to the invertebrate taste receptor family.LITE-1 strictly depends on protein conformation for photoabsorption,totally distinct from other photoreceptors found in metazoans,microbes,and plants.However,it remains unclear how does LITE-1 regulate this phototaxis response.Previous research showed that expression of lite-1 as a transgene in light insensitive body-wall muscles confers light sensitivity.To figure out the elaborate mechanism of how LITE-1 works to mediate light sensation in C.elegans,a forward genetic screen was performed in this study.Using light-induced contraction(i.e.paralysis)of LITE-1expressing muscles as a readout to screen for genes when mutated suppress LITE-1function,six candidates had been got in the end.One major group of lite-1 suppressors are the genes encoding thioredoxin reductase(trxr-1)and glutathione-disulfide reductase(gsr-1),which are required for regeneration of the two primary antioxidants thioredoxin and glutathione,suggesting that oxidization of LITE-1 inhibits its function.Further experiments demonstrated that the oxidant hydrogen peroxide(H₂O₂)suppresses phototaxis behavior and inhibits the photoresponse in photoreceptor neurons,whereas other sensory behaviors are relatively less vulnerable to H₂O₂.Conversely,antioxidants can rescue the phenotype of lite-1 suppressor mutants and promote the photoresponse.Similar results can be obtained by recording light-induced calcium response in the sensory neuron ASH.As UV light illumination generates H₂O₂,this study proposes that upon light activation of LITE-1,light-produced H₂O₂ then deactivates LITE-1 to terminate the photoresponse,while antioxidants may promote LITE-1's recovery from its inactive state.In conclusion,this study provides a potential mechanism by which H₂O₂ and antioxidants act synergistically to regulate photosensation in C.elegans.Compared with light transduction signaling in vertebrate and insect,the deactivation of LITE-1-mediated photoresponse in C.elegans is much simpler.In particular,UV light can deactivate the photoreceptor LITE-1 in time through H₂O₂produced by itself,which allow the photoreceptor to respond to subsequent light stimuli in an energy efficient way.Also,it shows that LITE-1 may be a direct target of H₂O₂.Although other sensory functions can also be impaired by H₂O₂,photosensation appears to be more vulnerable to this oxidant,which supports that H₂O₂at low concentrations has specific regulatory effect on many important physiological processes.