Haga Ken, Tsuchida-Mayama Tomoko, Yamada Mizuki, Sakai Tatsuya
Department of Human Science and Common Education, Nippon Institute of Technology, Miyashiro-cho, Minamisaitama-gun, Saitama 345-8501, Japan.
RIKEN Plant Science Center, Tsurumi-ku, Yokohama, Kanagawa 230-0045, Japan.
Plant Cell. 2015 Apr;27(4):1098-112. doi: 10.1105/tpc.15.00178. Epub 2015 Apr 14.
Living organisms adapt to changing light environments via mechanisms that enhance photosensitivity under darkness and attenuate photosensitivity under bright light conditions. In hypocotyl phototropism, phototropin1 (phot1) blue light photoreceptors mediate both the pulse light-induced, first positive phototropism and the continuous light-induced, second positive phototropism, suggesting the existence of a mechanism that alters their photosensitivity. Here, we show that light induction of ROOT PHOTOTROPISM2 (RPT2) underlies photosensory adaptation in hypocotyl phototropism of Arabidopsis thaliana. rpt2 loss-of-function mutants exhibited increased photosensitivity to very low fluence blue light but were insensitive to low fluence blue light. Expression of RPT2 prior to phototropic stimulation in etiolated seedlings reduced photosensitivity during first positive phototropism and accelerated second positive phototropism. Our microscopy and biochemical analyses indicated that blue light irradiation causes dephosphorylation of NONPHOTOTROPIC HYPOCOTYL3 (NPH3) proteins and mediates their release from the plasma membrane. These phenomena correlate closely with the desensitization of phot1 signaling during the transition period from first positive phototropism to second positive phototropism. RPT2 modulated the phosphorylation of NPH3 and promoted reconstruction of the phot1-NPH3 complex on the plasma membrane. We conclude that photosensitivity is increased in the absence of RPT2 and that this results in the desensitization of phot1. Light-mediated induction of RPT2 then reduces the photosensitivity of phot1, which is required for second positive phototropism under bright light conditions.
生物体通过在黑暗中增强光敏性以及在强光条件下减弱光敏性的机制来适应不断变化的光照环境。在胚轴向光性中,向光素1(phot1)蓝光光感受器介导脉冲光诱导的第一次正向光性和连续光诱导的第二次正向光性,这表明存在一种改变其光敏性的机制。在这里,我们表明根向光性2(RPT2)的光诱导是拟南芥胚轴向光性中光感受适应的基础。rpt2功能缺失突变体对极低光通量蓝光表现出增加的光敏性,但对低光通量蓝光不敏感。在黄化幼苗的向光性刺激之前表达RPT2会降低第一次正向光性期间的光敏性并加速第二次正向光性。我们的显微镜和生化分析表明,蓝光照射会导致非向光性胚轴3(NPH3)蛋白去磷酸化,并介导它们从质膜释放。这些现象与从第一次正向光性到第二次正向光性的过渡期内phot1信号的脱敏密切相关。RPT2调节NPH3的磷酸化,并促进质膜上phot1 - NPH3复合物的重建。我们得出结论,在没有RPT2的情况下光敏性增加,这导致phot1脱敏。然后光介导的RPT2诱导降低了phot1的光敏性,这是强光条件下第二次正向光性所必需的。