Environmental modulation of Arabidopsis light foraging strategies

作为不能选择环境的变温固着生物，植物必须使其生长和发育适应主要的环境条件。植物通过整合多种刺激来监测其周围环境，其中光和温度信号是最重要的。光信号被称为光敏色素的光感受器家族感知。在吸收红色波长后，光敏色素转化为它们的活性形式，抑制茎伸长并促进叶发育。然而，吸收远红波长会将光敏色素转换回其非活性形式。当生长在拥挤的群落中时，植物与邻近的植被竞争光来促进光合作用。相邻植被的存在被检测为从绿色组织反射或透射的光中的红色与远红色波长的比率（低R：FR比率）的减小。这种光质的变化导致遮荫植物中活性光敏色素的减少，并引发一系列被称为避荫综合征的伸长反应，通常以叶片发育为代价。这些反应有助于将叶子提升到树冠的间隙，并且可以在实验室中通过在补充有远红光波长的白色光下种植植物来研究。大多数已发表的实验使用超过20 ℃的生长温度来研究避荫反应。然而，当生长在较冷的温度下，拟南芥的叶片扩展响应低R：FR比例是惊人的逆转。与高R：FR比生长的对照相比，在16 oC下低R：FR比生长的植物显示出显著增加的叶面积、厚度和植物生物量。我们的观察结果表明，拟南芥显示可塑性的光觅食策略，每个策略的优先级由环境生长温度决定。在温度> 20 ℃时，拟南芥植物通过向冠层的间隙升高和伸长叶片/叶柄来寻找光线（避荫综合征1，SAS 1）。然而，在较低的温度下，采用了另一种策略，即植物大幅扩大叶面积和厚度，这可能会增加光子捕获（SAS 2）。在这个建议中，我们的目标是进行详细的分析，叶片解剖和光合性能的植物生长在高和低的R：FR比在广泛的生长温度。我们建议调查的可能性，不同的避荫策略是季节性的，通过实验在不加热的温室在多个季节。通过竞争和适应性实验，利用仅显示SAS 1的突变体和种质，研究了避荫策略中可塑性的适应价值。避荫策略中的自然遗传变异将利用QTL定位来鉴定基因组中负责这种变异的区域。这将最终能够识别参与这一过程的关键基因。此外，我们还观察到SAS 2和CBF调节子的表达的同时发生，CBF调节子是一组参与冷驯化和获得抗冻性的基因。因此，我们建议映射与低R：FR比介导的诱导CBF调节子的QTL，并与SAS 2确定的QTL进行比较。

As ectothermic, sessile organisms that cannot choose their surroundings, plants must adapt their growth and development to the prevailing environmental conditions. Plants monitor their surroundings by integrating multiple stimuli, of which light and temperature signals are the most important. Light signals are perceived using a family of photoreceptors named phytochromes. Upon absorption of red wavelengths, phytochromes are converted to their active form which inhibits stem elongation and promotes leaf development. Absorption of far-red wavelengths, however, converts phytochromes back to their inactive form. When growing in crowded communities, plants compete with neighbouring vegetation for light to fuel photosynthesis. The presence of neighbouring vegetation is detected as a reduction in the ratio of red to far red wavelengths (low R:FR ratio) in the light reflected from or transmitted through green tissues. This change in light quality results in a reduction in active phytochrome in shaded plants and initiates a suite of elongation responses termed the shade avoidance syndrome, often at the expense of leaf development. These responses serve to elevate leaves towards gaps in the canopy and can be studied in the laboratory by growing plants in white light supplemented with far-red wavelengths. The majority of published experiments use growth temperatures in excess of 20oC to study shade avoidance responses. When grown at cooler temperatures, however, the leaf expansion response of Arabidopsis to low R:FR ratio is strikingly reversed. Plants grown in low R:FR ratio at 16oC display significantly increased leaf area, thickness and plant biomass when compared to high R:FR ratio-grown controls. Our observations suggest that Arabidopsis displays plasticity in light foraging strategy with the precedence of each strategy being determined by ambient growth temperature. At temperatures >20oC, Arabidopsis plants forage for light by raising and elongating leaves/petioles towards gaps in the canopy (shade avoidance syndrome 1, SAS1). At cooler temperatures, however, an alternative strategy is adopted, whereby plants dramatically expand leaf area and thickness, which is likely to increase photon capture (SAS2). In this proposal we aim to perform detailed analyses of leaf anatomy and photosynthetic performance in plants grown in high and low R:FR ratio across a broad spectrum of growth temperatures. We propose to investigate the possibility that different shade avoidance strategies are seasonal through experiments in unheated glasshouses in multiple seasons. The adaptive value of plasticity in shade avoidance strategy will be investigated through competition and fitness experiments using mutants and accessions displaying only SAS1. Natural genetic variation in shade avoidance strategy will be exploited using QTL mapping to identify regions of the genome responsible for such variation. This will ultimately enable the identification of key genes involved in this process. In addition, we have observed co-incidence of SAS2 and expression of the CBF regulon, a suite of genes involved in cold acclimation and acquisition of freezing tolerance. We therefore propose to map QTLs associated with low R:FR ratio-mediated induction of the CBF regulon and compare with QTLs identified for SAS2.