Figure.7. Schematic diagram of rhodopsin transformation.
In the present study, long-wavelength sensitive LWS I andLWS II were found to be up-regulated in the O. oratoriacompound eye exposed to LCPL and we speculate that this is related to the shallow-water life habit ofO. oratoria (Sealifebase database). It is well-known that the penetration of long-wavelength light is not strong and thus it is mainly concentrated in the upper water (Chen et al., 2014). Both ultraviolet (UV)-sensitive SWS I and blue-sensitiveSWS II were also up-regulated in the O. oratoria compound eye exposed to LCPL. The polarization pattern in the UV and blue-ray have been speculated to be more stable and still trustworthy even in caliginous environment (Barta and Horváth, 2004; Horváth and Varjú, 2004). Meanwhile, both R7 and R8 retinular cells are UV-sensitive (Labhart and Meyer, 1999), and this property has been demonstrated to contribute to polarization vision in Musca domestica (von Philipsborn and Labhart, 1990) and Schistocerca gregaria (Schmeling et al., 2014). Accordingly, the SWS I andSWS II of the O. oratoria compound eye may be commonly used to detect the shorter-wavelength LCPL, and similar result has been confirmed in Neogonodactylus oerstedii (Portera et al., 2020). We also found ARR I , ARR II , TRPC , HISC andSLC to be up-regulated in the O. oratoria compound eye exposed to LCPL. The arrestin proteins encoded by the ARR I and ARR II have long been shown to control visual transduction cascades by deactivating the phosphorylated photopigments (Wilden et al., 1986; Liu et al., 2017), and thus the increased arrestins could maintain the animal’s ability to respond to light continuously (Renninger et al., 2011; Zang and Neuhauss, 2021). The transient receptor potential (TRP) channel involved by TRPC gene and histamine-gated chloride (HCL) channel involved by HISC gene are Ca2+ and Cl- permeable channels with pore canal, respectively, and have been shown to regulate the opening of cyclic nucleotide-gated ion channels during optical signaling and ultimately affect the photosensitivity (Geng et al., 2002; Leung et al., 2007). In fact, up-regulation of ion channel-related genes can result in a positive influence on retinal current, suggesting that ion channel-related genes are critical for the LCPL visual transmission (French et al., 2015). Notably, we identified another gene (KCNKN ) involved in ion channel regulation in the O. oratoria compound eye exposed to NL scenario. The KCNKN gene with K+ exchange function can balance the efflux/influx of Ca2+ in response to light stimulation, thus maintaining moderately high intracellular Ca2+ concentration (Sakurai et al., 2016; Vinberg et al., 2017). Additionally, the expression of RRHand CYAB were only up-regulated in the O. oratoriacompound eye under NL scenario. RRH -encoded peropsin is a chromophore like 11-cis-retinal, which can be bound to the all-trans retina and generate the 11-cis retina form under light stimulation (Koyanagi et al., 2002; Nagata et al., 2010). Therefore, peropsin can activate the transducin and has the function of light-sensing G protein-coupled receptors (Nagata et al., 2018).CYAB gene encodes the α-crytallin that has been shown to maintain crystalline lens transparency and phototaxis in vertebrates (Posner et al., 2012). Meanwhile, CYAB gene and sHSP (small heat shock protein) gene have also been confirmed to be sequentially homologous and possess molecular chaperone activity, which can be used to maintain the solubility of opsin and eventually effectively reduce light scattering in the O. oratoria compound eye.
Based on the potential function molecular responses of DEGs and DEPs described above, we can infer the CPLV transduction cascade processes in O. oratoria compound eyes (Figure.8). After the O. oratoria compound eye senses the LCPL, the 11-cis-retinal of the visual pigment isomerizes to trans-retinal and then detaches from shortwave opsin to activate shortwave opsin. Activated-shortwave-opsin is phosphorylated by G protein-coupled receptor kinase (GPK) and then binds to the transducin (T) that binding guanosine diphosphate (GDP). Subsequently, guanosine triphosphate (GTP) is exchanged with the GDP of the above complex and further produces T-GTP for activating the cyclic guanosine monophosphate-specific phosphodiesterase (cGMP-PDE). The protons produced by the hydrolysis of activated cGMP-PDE can inhibit sodium ion channels, resulting in nerve impulses and ultimately forming CPLV.