Department of Biological Sciences, University of Maryland Baltimore County, Baltimore, Maryland, United States of America.
Department of Ophthalmology, Gavin Herbert Eye Institute, University of California, Irvine, California, United States of America.
PLoS One. 2020 Apr 1;15(4):e0228121. doi: 10.1371/journal.pone.0228121. eCollection 2020.
Melanopsin is a visual pigment expressed in a small subset of ganglion cells in the mammalian retina known as intrinsically photosensitive retinal ganglion cells (ipRGCs) and is implicated in regulating non-image forming functions such as circadian photoentrainment and pupil constriction and contrast sensitivity in image formation. Mouse melanopsin's Carboxy-terminus (C-terminus) possesses 38 serine and threonine residues, which can potentially serve as phosphorylation sites for a G-protein Receptor Kinase (GRK) and be involved in the deactivation of signal transduction. Previous studies suggest that S388, T389, S391, S392, S394, S395 on the proximal region of the C-terminus of mouse melanopsin are necessary for melanopsin deactivation. We expressed a series of mouse melanopsin C-terminal mutants in HEK293 cells and using calcium imaging, and we found that the necessary cluster of six serine and threonine residues, while being critical, are insufficient for proper melanopsin deactivation. Interestingly, the additional six serine and threonine residues adjacent to the required six sites, in either proximal or distal direction, are capable of restoring wild-type deactivation of melanopsin. These findings suggest an element of plasticity in the molecular basis of melanopsin phosphorylation and deactivation. In addition, C-terminal chimeric mutants and molecular modeling studies support the idea that the initial steps of deactivation and β-arrestin binding are centered around these critical phosphorylation sites (S388-S395). The degree of functional versatility described in this study, along with ipRGC biophysical heterogeneity and the possible use of multiple signal transduction cascades, might contribute to the diverse ipRGC light responses for use in non-image and image forming behaviors, even though all six sub types of ipRGCs express the same melanopsin gene OPN4.
黑视蛋白是一种视觉色素,存在于哺乳动物视网膜的一小部分神经节细胞中,称为内在感光视网膜神经节细胞(ipRGC),并参与调节非成像功能,如昼夜节律光适应和瞳孔收缩以及图像形成中的对比敏感度。小鼠黑视蛋白的羧基末端(C 末端)具有 38 个丝氨酸和苏氨酸残基,这些残基可能作为 G 蛋白受体激酶(GRK)的磷酸化位点,并参与信号转导的失活。先前的研究表明,小鼠黑视蛋白 C 末端近端区域的 S388、T389、S391、S392、S394 和 S395 残基对于黑视蛋白失活是必需的。我们在 HEK293 细胞中表达了一系列小鼠黑视蛋白 C 末端突变体,并通过钙成像发现,虽然这六个必需的丝氨酸和苏氨酸残基对于黑视蛋白的适当失活是至关重要的,但它们是不充分的。有趣的是,在近端或远端方向上,与必需的六个位点相邻的另外六个丝氨酸和苏氨酸残基能够恢复野生型黑视蛋白的失活。这些发现表明,黑视蛋白磷酸化和失活的分子基础具有一定的可塑性。此外,C 末端嵌合突变体和分子建模研究支持这样一种观点,即失活和β-arrestin 结合的初始步骤集中在这些关键的磷酸化位点(S388-S395)周围。本研究中描述的功能多样性程度,以及 ipRGC 的生物物理异质性和可能使用多种信号转导级联,可能有助于不同的 ipRGC 光反应用于非成像和成像行为,即使所有六种 ipRGC 亚型都表达相同的黑视蛋白基因 OPN4。