The Control of Growth Symmetry Breaking in the Arabidopsis Hypocotyl
The Control of Growth Symmetry Breaking in the Arabidopsis Hypocotyl
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DOI：
10.1016/j.cub.2015.06.032
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发表时间：
2015-06
期刊：
影响因子：
9.2
通讯作者：
A. Peaucelle;R. Wightman;H. Höfte
中科院分区：
文献类型：
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作者：
A. Peaucelle;R. Wightman;H. Höfte
生物学中的复杂形状取决于细胞在发育过程中从各向同性生长转变为各向异性生长的能力。在植物中，这种生长对称性破坏反映了细胞壁延展性的变化。教科书的观点是，turgor-driven细胞扩张的方向取决于皮质微管（CMT）介导的纤维素微纤维的取向[1，2]。在这里，我们表明，这种观点充其量是不完整的。我们使用原子力显微镜（AFM）研究细胞壁力学的变化与生长对称性打破内下胚轴表皮。我们发现，首先，生长对称性破缺之前的纵向，横向，垂周壁相比，在没有变化的CMT取向的不对称松动。第二，这种壁松动是由纵向壁中的细胞壁果胶的选择性脱甲酯化引发的，第三，所产生的机械不对称性是生长对称性破坏所必需的。事实上，防止或促进果胶脱甲酯化，分别增加或减少了所有的细胞壁的刚度，但在这两种情况下，减少了生长各向异性。最后，我们表明，随后的CMT重新取向有助于巩固的增长轴，但不需要的增长对称性破缺。我们的结论是，生长对称性破缺控制在细胞尺度上由双极果胶脱甲酯化，而不是由纤维素依赖的机械各向异性的细胞壁本身。这种细胞不对称驱动的机制与植物中潜在的尖端生长相当[3]，但也与动物细胞中的各向异性细胞生长相当[4]。
Complex shapes in biology depend on the ability of cells to shift from isotropic to anisotropic growth during development. In plants, this growth symmetry breaking reflects changes in the extensibility of the cell walls. The textbook view is that the direction of turgor-driven cell expansion depends on the cortical microtubule (CMT)-mediated orientation of cellulose microfibrils [1, 2]. Here, we show that this view is incomplete at best. We used atomic force microscopy (AFM) to study changes in cell-wall mechanics associated with growth symmetry breaking within the hypocotyl epidermis. We show that, first, growth symmetry breaking is preceded by an asymmetric loosening of longitudinal, as compared to transverse, anticlinal walls, in the absence of a change in CMT orientation. Second, this wall loosening is triggered by the selective de-methylesterification of cell-wall pectin in longitudinal walls, and, third, the resultant mechanical asymmetry is required for the growth symmetry breaking. Indeed, preventing or promoting pectin de-methylesterification, respectively, increased or decreased the stiffness of all the cell walls, but in both cases reduced the growth anisotropy. Finally, we show that the subsequent CMT reorientation contributes to the consolidation of the growth axis but is not required for the growth symmetry breaking. We conclude that growth symmetry breaking is controlled at a cellular scale by bipolar pectin de-methylesterification, rather than by the cellulose-dependent mechanical anisotropy of the cell walls themselves. Such a cell asymmetry-driven mechanism is comparable to that underlying tip growth in plants [3] but also anisotropic cell growth in animal cells [4].