一个光敏色素B调控的水稻NBS-LRR基因的表达模式分析

利用水稻基因芯片比较野生型、phyA和phyB突变体受连续红光照射后的基因表达图谱,从中筛选到一个受光敏色素B(phyB)介导的红光信号特异诱导的、编码NBS-LRR类蛋白的基因,命名为PB-LRR(phyB-regulated NBS-LRR).为了揭示PB-LRR基因在水稻生长发育中的作用,对该基因表达的器官特异性...     

Arabidopsis Phytochrome D Is Involved in Red Light-Induced Negative Gravitropism of Hypocotyles

The phytochrome gene family, which is in Arabidopsis thaliana, consists of phytochromes A-E（phyA to phyE）, regulates plant responses to ambient light environments. PhyA and phyB have been characterized in detail, but studies on phyC to phyE have reported discrepant functions. In this study, we show that phyD regulates the Arabidopsis gravitropic response by inhibiting negative gravitropism of hypocotyls under red light condition. PhyD had only a limited effect on the gravitropic response of roots in red light condition. PhyD also enhanced phyB-regulated gravitropic responses in hypocotyls. Moreover, the regulation of hypocotyl gravitropic responses by phyD was dependent upon the red light fluence rate.     

Vision and development in Trichoderma atroviride

Phototropism, the induction of carotenogenesis and reproductive structures, and resetting of the circadian rhythm are controlled by blue light. Trichoderma is used as a photomorphogenetic model due to its ability to conidiate upon exposure to light. In total darkness, T. atroviride grows indefinitely as a mycelium provided that nutrients are not limiting. However, nutrient deprivation and light trigger the conidiation process. A pulse of blue light given to a radially growing colony induc…     

紫外光和蓝光调控查尔酮合成酶基因表达的研究

UV-B（280nm～320nm）、UV-A（320nm～390nm）和蓝光（390nm-500nm）经不同光受体和信号传递途径控制植物发育的各个方面。已知的蓝光／UV-A受体有隐花色素CRY1和CRY2，向光性受体有趋光素。氧化还原过程在隐花色素和趋光素信号转导过程中起重要作用。专一的UV-B光受体尚未被鉴定出，存在许多可能的UV-B信号传递途径．拟南芥查尔酮合成酶（CHS）的紫外光和蓝光转录调控成为研究热点。光受体突变体实验表明存在不同的UV-A／蓝光和UV-B光感知系统调控CHS的表达。拟南芥细胞悬浮培养物实验表明UV-B和CRY1信号传递途径在动力学上和药理学上不同。影响诱导CHS转录的启动子元件和转录因子现已被鉴定出。UV-B、隐花色素和光敏色素信号传递途径之间的相互作用调控CHS表达。UV-B途径与UV-A／蓝光途径的协同相互作用使CHS最大量表达。另外，专一的光敏色素经不同的增强和相巨作用正调控CRY1途径，负调控UV-B途径。     

Oxytocin selectively gates fear responses through distinct outputs from the central amygdala

Central amygdala (CeA) projections to hypothalamic and brain stem nuclei regulate the behavioral and physiological expression of fear, but it is unknown whether these different aspects of the fear response can be separately regulated by the CeA. We combined fluorescent retrograde tracing of CeA projections to nuclei that modulate fear-related freezing or cardiovascular responses with in vitro electrophysiological recordings and with in vivo monitoring of related behavioral and physiological parameters. CeA projections emerged from separate neuronal populations with different electrophysiological characteristics and different response properties to oxytocin. In vivo, oxytocin decreased freezing responses in fear-conditioned rats without affecting the cardiovascular response. Thus, neuropeptidergic signaling can modulate the CeA outputs through separate neuronal circuits and thereby individually steer the various aspects of the fear response.     

含PHYA基因的EDSV转移载体构建及表达研究

将原核表达载体pET30中的黑曲霉源植酸酶基因(phyA)亚克隆到真核表达载体pCDNA 3的kpaI-EcoRI位点。根据pCDNA 3的序列在增强子的上游(209位)和BGH polyA下游(2049位)设计1对引物HM 1,HM2扩增出含phyA基因的表达盒。将此表达盒以平末端连接的方式克隆到减蛋综合征病毒(EDSV)基因组右末端的转移载体pUHBC的Sall位点,酶切分析鉴定表达盒的方向,得到反向插入重组质粒pEDS-phyA。用Lipofectamine 2000将8μg pEDS-phyA转染90％满度的鸭胚成纤维细胞,6h后换生长液,24h后收获细胞,以puHBC转染作对照。钼酸胺法测定试验样品植酸酶酶活为977U／mL。实验结果表达我们已成功地构建了含植酸酶基因的转移载体,为进一步构建重组减蛋综合征病毒载体表达植酸酶打下基础。     

Myeloperoxidase,a leukocyte-derived vascular NO oxidase

Myeloperoxidase (MPO) is an abundant mammalian phagocyte hemoprotein thought to primarily mediate host defense reactions. Although its microbicidal functions are well established in vitro, humans deficient in MPO are not at unusual risk of infection. MPO was observed herein to modulate the vascular signaling and vasodilatory functions of nitric oxide (NO) during acute inflammation. After leukocyte degranulation, MPO localized in and around vascular endothelial cells in a rodent model of acute endotoxemia and impaired endothelium-dependent relaxant responses, to which MPO-deficient mice were resistant. Altered vascular responsiveness was due to catalytic consumption of NO by substrate radicals generated by MPO. Thus MPO can directly modulate vascular inflammatory responses by regulating NO bioavailability.