■植物生长是由内源遗传程序和环境线索控制的塑性现象。胚胎茎,下胚轴,由于其相对简单的几何形状和细胞组织,是定量研究增长的理想模型系统,以及它本质上单向的增长模式。拟南芥的下胚轴已经在分子遗传水平和细胞水平上得到了特别好的研究,它是分析避荫综合症(SAS)的首选模型,一种生长反应,使植物与邻近的植物竞争光。SAS期间,下胚轴生长主要由生长激素生长素控制,在不参与细胞分裂的情况下刺激细胞扩增。
■我们在生长素转运和生物合成缺陷的拟南芥突变体中评估了下胚轴生长的细胞分辨率,并基于已知的极性和非极性生长素转运蛋白(ABCB1,ABCB19和PIN)和控制下胚轴中生长素稳态的因素设计了一个数学生长素转运模型。此外,我们将基于精确细胞壁测量的细胞类型的生物物理特性引入模型。
■我们的模型可以基于子叶中产生的沿着下胚轴的生长素分布来生成观察到的细胞生长模式,沿着下胚轴运输,和生长素的一般营业额。这些原则,类似于动物形态发生梯度数学模型的特征,允许生成强大的浅层生长素梯度,因为它们预计存在于表现出定量生长素驱动的组织生长的组织中,与植物发育中模式机制产生的尖锐生长素最大值相反。
UNASSIGNED: Plant growth is a plastic phenomenon controlled both by endogenous genetic programs and by environmental cues. The embryonic stem, the hypocotyl, is an ideal model system for the quantitative study of growth due to its relatively simple geometry and cellular organization, and to its essentially unidirectional growth pattern. The hypocotyl of Arabidopsis thaliana has been studied particularly well at the molecular-genetic level and at the cellular level, and it is the model of choice for analysis of the shade avoidance syndrome (SAS), a growth reaction that allows plants to compete with neighboring plants for light. During SAS, hypocotyl growth is controlled primarily by the growth hormone auxin, which stimulates cell expansion without the involvement of cell division.
UNASSIGNED: We assessed hypocotyl growth at cellular resolution in Arabidopsis mutants defective in auxin transport and biosynthesis and we designed a mathematical auxin transport model based on known polar and non-polar auxin transporters (ABCB1, ABCB19, and PINs) and on factors that control auxin homeostasis in the hypocotyl. In addition, we introduced into the model biophysical properties of the cell types based on precise cell wall measurements.
UNASSIGNED: Our model can generate the observed cellular growth patterns based on auxin distribution along the hypocotyl resulting from production in the cotyledons, transport along the hypocotyl, and general turnover of auxin. These principles, which resemble the features of mathematical models of animal
morphogen gradients, allow to generate robust shallow auxin gradients as they are expected to exist in tissues that exhibit quantitative auxin-driven tissue growth, as opposed to the sharp auxin maxima generated by patterning mechanisms in plant development.