Environmental modulation of Arabidopsis light foraging strategies

植物是一种恒温的、无根的生物，不能选择周围的环境，植物必须适应周围的环境条件来生长和发育。植物通过整合多种刺激来监测周围环境，其中光和温度信号是最重要的。光信号是通过一组名为光敏色素的光感受器来感知的。在吸收红色波长后，光敏色素转化为活性形式，抑制茎伸长，促进叶片发育。然而，对远红色波长的吸收会将光敏色素转换回非活性形式。当植物生长在拥挤的群落中时，它们会与周围的植被竞争光来促进光合作用。从绿色组织反射或通过绿色组织透射的光中，红光与远红光波长的比值（低R:FR比值）降低，从而检测到邻近植被的存在。这种光质量的变化导致遮荫植物中活性光敏色素的减少，并启动一套称为遮荫回避综合征的伸长反应，通常以牺牲叶片发育为代价。这些反应有助于将叶片抬升到树冠的缝隙处，可以在实验室中通过在白光和远红光的补充下种植植物来研究。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避荫反应。然而，当生长温度较低时，拟南芥对低R:FR的叶片扩张响应明显相反。在16℃低R:FR条件下生长的植株与高R:FR条件下生长的对照相比，叶片面积、厚度和生物量显著增加。我们的观察表明，拟南芥在光觅食策略上表现出可塑性，每种策略的优先级由环境生长温度决定。在0 ~ 20℃的温度下，拟南芥植物通过向树冠间隙伸长和伸长叶片/叶柄来获取光照（遮荫回避综合征1，SAS1）。然而，在较低的温度下，植物采用了另一种策略，即植物显著扩大叶子面积和厚度，这可能会增加光子捕获（SAS2）。在本提案中，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比下的植物的叶片解剖和光合性能进行详细分析。我们建议通过在不同季节的无加热温室中进行实验来研究不同遮阳策略的季节性可能性。我们将通过竞争和适应度实验，研究只显示SAS1的突变体和品种在避荫策略中的适应性价值。利用QTL作图来确定导致这种变异的基因组区域，将利用避荫策略中的自然遗传变异。这将最终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调控的表达同时发生，CBF调控是一组参与冷驯化和耐寒性获得的基因。因此，我们建议绘制与低R:FR比率介导的CBF调控诱导相关的qtl，并与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.