北京大学的邓兴旺（Xing Wang Deng）教授是世界著名的生物学家，其长期从事植物分子遗传及生理学方面的研究，多次在Cell、Science、Nature等世界权威刊物上发表很有影响的学术文章。并于去年当选为美国科学院院士。本月，邓兴旺教授课题组接连在《美国国家科学院院刊》（PNAS）上发表了两篇研究论文，探讨了光形态建成（photomorphogenesis）的调控机制。

光是自然界中影响植物生长发育的最重要的环境因素之一。植物不仅通过光合作用将光能转化成化学能储存起来，光还能以信息的形式作用于植物并调节植物的分化、生长、发育，使其更好地适应外界环境。

这种调节通过生物膜系统结构、透性的变化和/或基因表达的变化促成细胞的分化及结构和功能的改变，最终汇集成组织和器官的建成，就是光形态建成，亦即光控发育或光信号传导的过程。近年来，由于现代生物化学和分子生物学的发展，光形态建成成为了植物发育生物学的一个热点。

众所周知，长波长、低能量的紫外线B （UV-B光）是诱导植物光形态建成的一个重要信号。在过去的十年里，科学家们以拟南芥作为模式植物，采用遗传性和分子方法揭示出了与许多UV-B光特异性信号相关的因子，其中包括UV-B光线受体UVR8；正调控因子COP1和HY5;以及负调控因子cullin4、RUP1和RUP2。然而，到目前为止都还未系统地了解整个光形态建成UV-B信号网络。

在发表于7月21日，题为“Coordinated photomorphogenic UV-B signaling network captured by mathematical modeling”的论文中，研究人员报告称他们结合数学模型和生物学实验，阐析了UV-B光信号传导中不同信号通路的协调机制。揭示了在早期及持续长时间响应致形态发生的UV-B光过程中不同蛋白质复合物之间的功能互作。

而在另一篇题为“Arabidopsis noncoding RNA mediates control of photomorphogenesis by red light”的文章中，研究人员则鉴别出了拟南芥的一个非编码RNA：HID1（HIDDEN TREASURE 1）促进了持续红光下光形态建成。并且证实HID1是通过PIF3来发挥这一作用的，PIF3编码了已知是光形态建成关键抑制物的一个碱性螺旋转录因子。此外，他们还证实HID似乎高度保守地存在于高等植物中。研究人员认为HID1这一新型非编码RNA的功能，代表了对幼苗光形态建成另一个层次的精确调控。(引自：生物谷360)

Coordinated photomorphogenic UV-B signaling network captured

 by mathematical modeling

Abstract  Long-wavelength and low-fluence UV-B light is an informational signal known to induce photomorphogenic development in plants. Using the model plant Arabidopsis thaliana, a variety of factors involved in UV-B–specific signaling have been experimentally characterized over the past decade, including the UV-B light receptor UV resistance locus 8; the positive regulators constitutive photomorphogenesis 1 and elongated hypocotyl 5; and the negative regulators cullin4, repressor of UV-B photomorphogenesis 1 (RUP1), and RUP2. Individual genetic and molecular studies have revealed that these proteins function in either positive or negative regulatory capacities for the sufficient and balanced transduction of photomorphogenic UV-B signal. Less is known, however, regarding how these signaling events are systematically linked. In our study, we use a systems biology approach to investigate the dynamic behaviors and correlations of multiple signaling components involved in Arabidopsis UV-B–induced photomorphogenesis. We define a mathematical representation of photomorphogenic UV-B signaling at a temporal scale. Supplemented with experimental validation, our computational modeling demonstrates the functional interaction that occurs among different protein complexes in early and prolonged response to photomorphogenic UV-B.

原文链接：http://www.pnas.org/content/early/2014/07/16/1412050111.full.pdf+html?with-ds=yes

Arabidopsis noncoding RNA mediates control of photomorphogenesis

 by red light

Abstract  Seedling photomorphogenesis is a sophisticated developmental process that is controlled by both the transcriptional and posttranscriptional regulation of gene expression. Here, we identify an Arabidopsis noncoding RNA, designated HIDDEN TREASURE 1 (HID1), as a factor promoting photomorphogenesis in continuous red light (cR). We show that HID1 acts through PHYTOCHROME-INTERACTING FACTOR 3 (PIF3), which encodes a basic helix–loop–helix transcription factor known to be a key repressor of photomorphogenesis. Knockdown of HID1 in hid1 mutants leads to a significant increase in the expression of PIF3, which in turn drives the development of elongated hypocotyls in cR. We identified two major stem-loops in HID1 that are essential for its modulation of hypocotyl growth in cR-grown seedlings. Furthermore, our data reveal that HID1 is assembled into large nuclear protein–RNA complex(es) and that it associates with the chromatin of the first intron of PIF3 to repress its transcription. Strikingly, phylogenetic analysis reveals that many land plants have conserved homologs of HID1 and that its rice homolog can rescue the mutant phenotype when expressed in Arabidopsis hid1 mutants. We thus concluded that HID1 is a previously uncharacterized noncoding RNA whose function represents another layer of regulation in the precise control of seedling photomorphogenesis.

原文链接：http://www.pnas.org/content/111/28/10359.full.pdf+html?with-ds=yes