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.