Expression Patterns of OsPIL11,a Phytochrome-Interacting Factor in Rice,and Preliminary Analysis of Its Roles in Light Signal Transduction

The expression patterns of OsPILll, one of six putative phytochrome-interacting factors, were analyzed in different organs of transgenic tobacco （Nicotiana tabacum）. The expression of OsPIL 11 was organ-specific and was regulated by leaf development, abscisic acid （ABA）, jasmonic acid （JA） and salicylic acid （SA）. To further explore the role of OsPIL 11 in plant light signal transduction, a plant expression vector of OsPILll was constructed and introduced into tobacco. When grown under continuous red light, OsPILll-overexpressed transgenic tobacco exhibited shorter hypocotyls and larger cotyledons and leaves compared to wild-type seedlings. When grown under continuous far-red light, however, transgenic and wild-type seedlings showed similar phenotypes. These results indicate that OsPILll is involved in red light induced de-etiolation, but not in far-red light induced de-etiolation in transgenic tobacco, which lays the foundation for dissecting the function of OsPIL11 in phytochrome-mediated light signal transduction in rice.

Study of light signal receptor of Stephanopyxis palmeriana during sexual reproduction

We collected centric diatom Stephanopyxis palmeriana samples in coastal waters of Xiamen for charac- teristic red light/far red light (R/FR) phytochrome reactions to identify its photoreceptor in the course of sexual repro- duction. The result showed that pre-illumination of 2-3h red light before darkness could induce sexualization of S. palmeriana, while the follow-up illumination of far red light could reverse the effect of red light, which is a featured reaction of phytochrome. The Southern Dot Blot was carried out to identify the type of phytochrome that induces the sexualization. The result also showed high homogeneity of DNA fragment of S. palmeriana with phyB, but phyA. This means the photoreceptor in the process of sexual reproduction of S. palmeriana is phytochrome B (phyB).

Regulated Degradation of HFR1 Desensitizes Light Signaling in Arabidopsis

Arabidopsis seedlings undergo photomorphogenesis in the light and etiolation in the dark. HFR1, a bHLH transcription factor, is required for both phytochrome A (phyA)-mediated far-red and cryptochrome 1 (cry1)-mediated blue light signaling. We report that HFR1 is a short-lived protein in darkness and is degraded through a 26S proteasome-dependent pathway. Light, irrespective of its quality, enhances HFR1 protein accumulation via promoting its stabilization. We demonstrate that HFR1 physically interacts with COP1 and that COP1 exhibits ubiquitin ligase activity toward HFR1 in vitro. In addition, we show that COP1 is required for degradation of HFR1 in vivo. Furthermore, plants overexpressing a C-terminal 161 amino acid fragment of HFR1 (CT161) display enhanced photomorphogenesis, suggesting an autonomous function of CT161 in promoting light signaling. This truncated HFR1 gene product is more stable than the full-length HFR1 protein in darkness, indicating that the COP1-interacting N-terminal portion of HFR1 is essential for COP1-mediated destabilization of HFR1. These results suggest that light enhances HFR1 protein accumulation by abrogating COP1-mediated degradation of HFR1, which is necessary and sufficient for promoting light signaling. Additionally, our results substantiate the E3 ligase activity of COP1 and its critical role in desensitizing light signaling.

Modulation of starch synthesis in Arabidopsis via phytochrome B-mediated light signal transduction

Starch is a major storage carbohydrate in plants and is critical in crop yield and quality.Starch synthesis is intricately regulated by internal metabolic processes and external environmental cues;however,the precise molecular mechanisms governing this process remain largely unknown.In this study,we revealed that high red to far-red(high R:FR)light significantly induces the synthesis of leaf starch and the expression of synthesis-related genes,whereas low R:FR light suppress these processes.Arabidopsis phytochrome B(phyB),the primary R and FR photoreceptor,was identified as a critical positive regulator in this process.Downstream of phyB,basic leucine zipper transcription factor ELONGATED HYPOCOTYL5(HY5)was found to enhance starch synthesis,whereas the basic helix-loop-helix transcription factors PHYTOCHROME INTERACTING FACTORs(PIF3,PIF4,and PIF5)inhibit starch synthesis in Arabidopsis leaves.Notably,HY5 and PIFs directly compete for binding to a shared G-box cis-element in the promoter region of genes encoding starch synthases GBSS,SS3,and SS4,which leads to antagonistic regulation of their expression and,consequently,starch synthesis.Our findings highlight the vital role of phyB in enhancing starch synthesis by stabilizing HY5 and facilitating PIFs degradation under high R:FR light conditions.Conversely,under low R:FR light,PIFs predominantly inhibit starch synthesis.This study provides insight into the physiological and molecular functions of phyB and its downstream transcription factors HY5 and PIFs in starch synthesis regulation,shedding light on the regulatory mechanism by which plants synchronize dynamic light signals with metabolic cues to module starch synthesis.

RACK1A promotes hypocotyl elongation by scaffolding light signaling components in Arabidopsis

Plants deploy versatile scaffold proteins to intricately modulate complex cell signaling.Among these,RACK1A(Receptors for Activated C Kinase 1A)stands out as a multifaceted scaffold protein functioning as a central integrative hub for diverse signaling pathways.However,the precise mechanisms by which RACK1A orchestrates signal transduction to optimize seedling development remain largely unclear.Here,we demonstrate that RACK1A facilitates hypocotyl elongation by functioning as a flexible platform that connects multiple key components of light signaling pathways.RACK1A interacts with PHYTOCHROME INTERACTING FACTOR(PIF)3,enhances PIF3 binding to the promoter of BBX11 and down-regulates its transcription.Furthermore,RACK1A associates with ELONGATED HYPOCOTYL 5(HY5)to repress HY5 biochemical activity toward target genes,ultimately contributing to hypocotyl elongation.In darkness,RACK1A is targeted by CONSTITUTIVELY PHOTOMORPHOGENIC(COP)1 upon phosphorylation and subjected to COP1-mediated degradation via the 26 S proteasome system.Our findings provide new insights into how plants utilize scaffold proteins to regulate hypocotyl elongation,ensuring proper skoto-and photo-morphogenic development.

BZS1, a B-box Protein, Promotes Photomorphogenesis Downstream of Both Brassinosteroid and Light Signaling Pathways

Photomorphogenesis is controlled by multiple signaling pathways, including the light and brassinosteroid （BR） pathways. BR signaling activates the BZR1 transcription factor, which is required for suppressing photomorphogen- esis in the dark, We identified a suppressor of the BR hypersensitive mutant bzrl-lD and named it bzrl-lD suppressorl- Dominant （bzsl-D）. The bzsl-D mutation was caused by overexpression of a B-box zinc finger protein BZS1, which is transcriptionally repressed by BZR1. Overexpression of BZS1 causes de-etiolation in the dark, short hypocotyls in the light, reduced sensitivity to BR treatment, and repression of many BR-activated genes. Knockdown of BZS1 by co-suppression partly suppressed the short hypocotyl phenotypes of BR-deficient or insensitive mutants. These results support that BZSl is a negative regulator of BR response. BZS1 overexpressors are hypersensitive to different wavelengths of light and loss of function of BZS1 reduces plant sensitivity to light and partly suppresses the constitutive photomorphogenesis 1 （cop1） mutant in the dark, suggesting a positive role in light response. BZS1 protein accumulates at an increased level after light treatment of dark-grown BZSl-OXplants and in the cop1 mutants, and BZS1 interacts with COP1 in vitro, suggesting that light regulates BZS1 through COPl-mediated ubiquitination and proteasomal degradation. These results demonstrate that BZS1 mediates the crosstalk between BR and light pathways.

Coordination of Plastid and Light Signaling Pathways upon Development of Arabidopsis Leaves under Various Photoperiods

Plants synchronize their cellular and physiological functions according to the photoperiod （the length of the light period） in the cycle of 24 h. Photoperiod adjusts several traits in the plant life cycle, including flowering and senes- cence in annuals and seasonal growth cessation in perennials. Photoperiodic development is controlled by the coordinated action of photoreceptors and the circadian clock. During the past 10 years, remarkable progress has been made in under- standing the molecular mechanism of the circadian clock, especially with regard to the transition of Arabidopsis from the vegetative growth to the reproductive phase. Besides flowering photoperiod also modifies plant photosynthetic struc- tures and traits. Light signals controlling biogenesis of chloroplasts and development of leaf photosynthetic structures are perceived both by photoreceptors and in chloroplasts. In this review, we provide evidence suggesting that the photope- riodic development of Arabidopsis leaves mimics the acclimation of plant to various light intensities. Furthermore, the chloroplast-to-nucleus retrograde signals that adjust acclimation to light intensity are proposed to contribute also to the signaling pathways that control photoperiodic acclimation of leaves.

Long-distance blue light signalling regulates phosphate deficiency-induced primary root growth inhibition

Although roots are mainly embedded in the soil, recent studies revealed that light regulates mineral nutrient uptake by roots. However, it remains unclear whether the change in root system architecture in response to different rhizosphere nutrient statuses involves light signaling. Here, we report that blue light regulates primary root growth inhibition under phosphate-deficient conditions through the cryptochromes and their downstream signaling factors. We showed that the inhibition of root elongation by low phosphate requires blue light signal perception at the shoot and transduction to the root. In this process, SPA1 and COP1 play a negative role while HY5 plays a positive role. Further experiments revealed that HY5 is able to migrate from the shoot to root and that the shoot-derived HY5 autoactivates root HY5 and regulates primary root growth by directly activating the expression of LPR1, a suppressor of root growth under phosphate starvation. Taken together, our study reveals a regulatory mechanism by which blue light signaling regulates phosphate deficiency-induced primary root growth inhibition, providing new insights into the crosstalk between light and nutrient signaling.

Coordinated Shoot and Root Responses to Light Signaling in Arabidopsis

Light is one of the most important environmental signals and regulates many biological processes in plants.Studies on light-regulated development have mainly focused on aspects of shoot growth,such as deetiolation,cotyledon opening,inhibition of hypocotyl elongation,flowering,and anthocyanin accumulation.However,recent studies have demonstrated that light is also involved in regulating root growth and development in Arabidopsis.In this review,we summarize the progress in understanding how shoots and roots coordinate their responses to light through different light-signaling components and pathways,including the COP1(CONSTITUTIVELY PHOTOMORPHOGENIC 1),HY5(ELONGATED HYPOCOTYL 5),and MYB73/MYB77(MYB DOMAIN PROTEIN 73/77)pathways.

The involvement of the N-terminal PHR domain of Arabidopsis cryptochromes in mediating light signaling

Light is a key environmental cue that fundamentally regulates all aspects of plant growth and development,which is mediated by the multiple photoreceptors including the blue light photoreceptors cryptochromes(CRYs).In Arabidopsis,there are two well-characterized homologous CRYs,CRY1 and CRY2.Whereas CRYs are flavoproteins,they lack photolyase activity and are characterized by an Nterminal photolyase-homologous region(PHR)domain and a C-terminal extension domain.It has been established that the C-terminal extension domain of CRYs is involved in mediating light signaling through direct interactions with the master negative regulator of photomorphogenesis,COP1.Recent studies have revealed that the N-terminal PHR domain of CRYs is also involved in mediating light signaling.In this review,we mainly summarize and discuss the recent advances in CRYs signaling mediated by the N-terminal PHR domain,which involves the N-terminal PHR domain-mediated dimerization/oligomerization of CRYs and physical interactions with the pivotal transcription regulators in light and phytohormone signaling.

A Workable Solution for Reducing the Large Number of Vehicle and Pedestrian Accidents Occurring on a Yellow Light

Traffic intersections are incredibly dangerous for drivers and pedestrians. Statistics from both Canada and the U.S. show a high number of fatalities and serious injuries related to crashes at intersections. In Canada, during 2019, the National Collision Database shows that 28% of traffic fatalities and 42% of serious injuries occurred at intersections. Likewise, the U.S. National Highway Traffic Administration (NHTSA) found that about 40% of the estimated 5,811,000 accidents in the U.S. during the year studied were intersection-related crashes. In fact, a major survey by the car insurance industry found that nearly 85% of drivers could not identify the correct action to take when approaching a yellow traffic light at an intersection. One major reason for these accidents is the “yellow light dilemma,” the ambiguous situation where a driver should stop or proceed forward when unexpectedly faced with a yellow light. This situation is even further exacerbated by the tendency of aggressive drivers to inappropriately speed up on the yellow just to get through the traffic light. A survey of Canadian drivers conducted by the Traffic Injury Research Foundation found that 9% of drivers admitted to speeding up to get through a traffic light. Another reason for these accidents is the increased danger of making a left-hand turn on yellow. According to the National Highway Traffic Safety Association (NHTSA), left turns occur in approximately 22.2% of collisions—as opposed to just 1.2% for right turns. Moreover, a study by CNN found left turns are three times as likely to kill pedestrians than right turns. The reason left turns are so much more likely to cause an accident is because they take a driver against traffic and in the path of oncoming cars. Additionally, most of these left turns occur at the driver’s discretion—as opposed to the distressingly brief left-hand arrow at busy intersections. Drive Safe Now proposes a workable solution for reducing the number of accidents occurring during a yellow light at intersections. We believe this fairly simple solution will save lives, prevent injuries, reduce damage to public and private property, and decrease insurance costs.

Light regulation of horticultural crop nutrient uptake and utilization

Plants demonstrate dynamic changes in molecular structures under fluctuating light conditions.Accumulating evidence suggests that light plays a vital role in plant growth and morphogenesis.In particular,light has a role in the absorption and utilization of nutrients in plants.Despite significant progress in understanding the mechanism of nutrient acquisition and assimilation,how light affects and regulates ion uptake remains a question.Studies in model plants,Arabidopsis thaliana,suggest that light affects the nutrient utilization in roots through a complex regulatory network;nonetheless,the molecular mechanisms underlying the various effects of light on these processes in crop plants remain fragmentary.In this review,we discuss the light effects(light quality,light intensity,and photoperiod)on nutrient uptake and utilization in horticultural crops for optimizing crop productivity and increasing fertilizer use efficiency.

基于LIGHT-HVEM信号通路探讨健脾养血祛风方对脾虚型慢性湿疹小鼠作用机制

目的基于肿瘤坏死因子超家族第14个成员(LIGHT)-疱疹病毒入侵介质(HVEM)信号通路探讨健脾养血祛风方对脾虚型慢性湿疹小鼠的作用机制。方法60只雄性昆明小鼠随机分为空白对照组10只和模型组50只。模型组采用小剂量二硝基氯苯(DNCB)反复涂抹联合番泻叶灌服建立脾虚型慢性湿疹小鼠模型。造模成功的50只小鼠随机分成模型对照组、西药治疗组、中药低剂量治疗组、中药中剂量治疗组和中药高剂量治疗组,每组10只。西药治疗组予盐酸左西替利嗪片灌胃,中药各剂量组予健脾养血祛风方灌胃,空白对照组和模型对照组予等体积生理盐水灌胃,各组均连续给药14 d。观察背部皮肤肿胀度和组织形态学变化,检测血清白细胞介素2(IL-2)、白细胞介素6(IL-6)、肿瘤坏死因子α(TNF-α)表达水平,皮肤LIGHT、HVEM蛋白表达水平。结果与空白对照组比较,模型对照组小鼠皮肤肿胀度和血清IL-2、IL-6、TNF-α表达水平显著升高(P<0.01),皮肤组织形态学表现呈现慢性湿疹病理改变,皮肤LIGHT、HVEM蛋白表达水平显著升高(P<0.01);与模型对照组比较,西药治疗组、中药高剂量治疗组小鼠皮肤肿胀度和血清IL-2、IL-6、TNF-α表达水平显著降低(P<0.05或P<0.01),皮肤组织形态学表现明显改善,西药治疗组、中药治疗组皮肤LIGHT、HVEM蛋白表达水平显著降低(P<0.01)。结论健脾养血祛风方对脾虚型慢性湿疹小鼠具有抗炎和免疫调节作用,以高剂量效果最佳,其作用机制可能是通过抑制LIGHT-HVEM信号通路,降低血清IL-2、IL-6、TNF-α表达水平,调节Th1/Th2细胞因子动态平衡,从而有效改善皮肤肿胀度和皮肤组织病理形态。

人重组LIGHT-Fc分子的真核表达及其抗肿瘤活性研究

目的 :构建人LIGHT Fc基因的真核表达质粒 ,并表达获得有较高生物学活性的纯化人LIGHT Fc融合蛋白。方法 :从cDNA文库中PCR扩增LIGHT全长编码基因 ,并导入克隆载体。测序证实后 ,继续用PCR扩增其膜外区cDNA ,用重叠延伸技术(SOE)引入CD137信号肽基因。将SOE产物与hIgG1Fc基因一起装入真核表达载体pcDNA3中 ,瞬时转染 2 93T细胞 ,用夹心ELISA检测其表达情况 ,经蛋白A亲和纯化 ,用SDS PAGE检测其纯度与Mr,并以肿瘤细胞为靶细胞 ,检测其生物学活性。结果 :测序证实构建的LIGHT与LIGHT FccDNA阅读框完整 ,连接部位序列正确 ;ELISA和SDS PAGE证实LIGHT Fc融合蛋白的表达与纯度 ;MTT证明人LIGHT Fc蛋白对一些肿瘤细胞系具有生长抑制作用。结论 :获得了有抗肿瘤活性的纯化hLIGHT Fc融合蛋白 ,为探讨LIGHT在免疫自稳调节中的地位、结合相应受体后的动力学与信号转导机制 。

SVC Light次同步振荡阻尼特性分析

以绝缘栅双极晶闸管(IGBT)和脉宽调制(PWM)控制为基础的新型静止无功补偿装置(SVC Light),可快速调节其与交流系统间交换的感性或容性无功功率,具有提高振荡阻尼特性的能力。介绍SVC Light的工作原理,推导出三相abc坐标系下的数学模型,建立基于受控电压源和受控电流源的等效仿真模型,并设计出基于比例-积分调节器的直流电压、无功功率和交流母线电压控制器。利用复转矩系数的时域实现方法——测试信号法,分析SVC Light不同控制方式、主电路参数以及控制器参数对发电机电气阻尼特性的影响。研究结果表明,SVC Light在配置次同步附加阻尼控制器后,通过动态调节其与交流系统间交换的无功功率,可以显著增加发电机电气阻尼,有效抑制由串联电容补偿引发的发电机轴系振荡。

基于ESPRIT-PSA与LightGBM算法的感应电动机转子断条数目诊断新方法

提出一种基于旋转不变信号参数估计技术ESPRIT(Estimation of signal parameters via rotational invariance technique)、模式搜索算法PSA(Pattern search algorithm)与轻型梯度提升机LightGBM(Light gradient boosting machine)结合的感应电动机转子断条数目诊断新方法。模拟了转子断条故障下的瞬时无功功率信号并用其衡量ESPRIT-PSA的性能。结果表明:ESPRIT-PSA只需短时数据就能准确测量瞬时无功功率信号中的转子断条故障特征分量。随后,为解决现有的电机瞬时无功功率信号分析MIRPSA(Motor instantaneous reactive power signal analysis)类方法无法准确诊断转子断条数目的问题,引入LightGBM对转子断条故障进行多分类以准确诊断转子断条数目。最后针对一台异步电动机进行转子断条诊断实验,结果表明:该方法是有效的,并且因将瞬时无功功率作为分析信号而适用于电机低转差率的情况。

CD160/BTLA-HVEM-LIGHT/LT-α共信号通路与单纯疱疹病毒性角膜基质炎的研究

单纯疱疹病毒性角膜基质炎（HSK）是主要由CD4^＋ T细胞介导的免疫病理性疾病，是可致盲的角膜感染性疾病之一。单纯疱疹病毒（HSV）进入介导子（HVEM）又名TNFRSF14，在病毒感染时可以通过病毒表面糖蛋白D（gD）介导HSV进入细胞。目前研究证实存在5种配体与HVEM结合，分别为HSV-gD、BALT、CD160、LIGHT和淋巴毒素α（LT-α）。HSV-gD与HVEM结合能够促进病毒包膜与细胞的融合，介导病毒在细胞间的扩散和释放。在T细胞的活化和增生中，HVEM-LIGHT/LT-α提供协同刺激信号，HVEM-BTLA/CD160提供协同抑制信号，此双向作用使HVEM成为一个＂分子开关＂，共同调节机体免疫应答。本文分别阐述HVEM通过与不同的配体结合所发挥不同的生物学作用，并结合CD160/BTLA-HVEM-LIGHT/LT-α共信号通路在HSK的相关实验研究，深入了解HSK的发病机制，并为HSK的有效治疗提供思路。通过有效的临床干预降低炎性免疫反应，从而达到对自身免疫性疾病的复发和慢性免疫性疾病的治疗作用。

Resolution and noise in ghost imaging with classical thermal light

The resolution and classical noise in ghost imaging with a classical thermal light are investigated theoretically. For ghost imaging with a Gaussian Schell model source, the dependences of the resolution and noise on the spatial coherence of the source and the aperture in the imaging system are discussed and demonstrated by using numerical simulations. The results show that an incoherent source and a large aperture will lead to a good image quality and small noise.

Technique of Position Sensitive Detector with Alternating Light Source

The signal processing circuits of position sensitive detector(PSD) with alternating light source are presented.The measuring device of PSD with alternating light source can effectively eliminate the interference made by light noise signal.

Puerarin protects rat brain against ischemia/reperfusion injury by suppressing autophagy via the AMPK-mT OR-ULK1 signaling pathway

Puerarin suppresses autophagy to alleviate cerebral ischemia/reperfusion injury, and accumulating evidence indicates that the AMPKm TOR signaling pathway regulates the activation of the autophagy pathway through the coordinated phosphorylation of ULK1. In this study, we investigated the mechanisms underlying the neuroprotective effect of puerarin and its role in modulating autophagy via the AMPK-m TOR-ULK1 signaling pathway in the rat middle cerebral artery occlusion model of cerebral ischemia/reperfusion injury. Rats were intraperitoneally injected with puerarin, 50 or 100 mg/kg, daily for 7 days. Then, 30 minutes after the final administration, rats were subjected to transient middle cerebral artery occlusion for 90 minutes. Then, after 24 hours of reperfusion, the Longa score and infarct volume were evaluated in each group. Autophagosome formation was observed by transmission electron microscopy. LC3, Beclin-1 p62, AMPK, m TOR and ULK1 protein expression levels were examined by immunofluorescence and western blot assay. Puerarin substantially reduced the Longa score and infarct volume, and it lessened autophagosome formation in the hippocampal CA1 area following cerebral ischemia/reperfusion injury in a dose-dependent manner. Pretreatment with puerarin（50 or 100 mg/kg） reduced Beclin-1 expression and the LC3-II/LC3-I ratio, as well as p-AMPK and p S317-ULK1 levels. In comparison, it increased p62 expression. Furthermore, puerarin at 100 mg/kg dramatically increased the levels of p-m TOR and p S757-ULK1 in the hippocampus on the ischemic side. Our findings suggest that puerarin alleviates autophagy by activating the APMK-m TOR-ULK1 signaling pathway. Thus, puerarin might have therapeutic potential for treating cerebral ischemia/reperfusion injury.