Environmental modulation of Arabidopsis light foraging strategies

作为不能选择周围环境的外温固着生物，植物必须使自己的生长和发育适应当时的环境条件。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。光信号是通过一系列名为光敏色素的光感受器来感知的。当吸收红色波长时，光敏色素转化为活性形式，抑制茎的伸长，促进叶片的发育。然而，对远红光波长的吸收会将光敏色素转换回不活跃的形式。当生长在拥挤的群落中时，植物会与邻近的植被争夺光能，以促进光合作用。邻近植被的存在被检测为从绿色组织反射或透过绿色组织的光中红光与远红光波长的比率(低R：FR比率)的减少。这种光质的变化导致遮荫植物中活性光敏色素的减少，并引发一系列称为遮荫回避综合症的伸长反应，通常以叶片发育为代价。这些反应有助于将叶片抬高到树冠上的缝隙，并可以在实验室通过在白光和远红波长的补充下种植植物来进行研究。大多数已发表的实验使用超过20摄氏度的生长温度来研究遮荫反应。然而，当在较低的温度下生长时，拟南芥对低R：FR比的叶片扩展反应显著逆转。与高R：FR比的对照相比，低R：FR比在16oC下生长的植株表现出显著的叶面积、厚度和植株生物量的增加。我们的观察表明，拟南芥在光觅食策略上表现出可塑性，每种策略的优先顺序取决于环境生长温度。在&gt；20oC的温度下，拟南芥植物通过抬高和拉长叶片/叶柄朝向树冠上的缝隙来觅光(遮荫回避综合症1，SAS1)。然而，在温度较低的情况下，采用了另一种策略，即植物极大地扩大叶面积和厚度，这可能会增加光子捕获(SAS2)。在这项建议中，我们的目标是在广泛的生长温度范围内，对生长在高R：FR比和低R：FR比的植物的叶片解剖和光合作用表现进行详细的分析。我们建议通过在不加热的温室中进行多个季节的实验来研究不同的遮荫回避策略具有季节性的可能性。利用只显示SAS1的突变体和材料，通过竞争和适应度实验，研究可塑性在遮荫策略中的适应性价值。遮荫策略中的自然遗传变异将被利用QTL作图来确定基因组中负责这种变异的区域。这最终将使识别参与这一过程的关键基因成为可能。此外，我们还观察到SAS2和CBF调节子的共同出现，CBF调节子是一组参与冷驯化和获得耐寒性的基因。因此，我们建议定位与低R：FR比率介导的CBF调节子诱导相关的QTL，并与已发现的SAS2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.