Transcriptional induction of cell wall remodelling genes is coupled to microtubule-driven growth isotropy at the shoot apex in Arabidopsis.

The shoot apical meristem of higher plants continuously generates new tissues and organs through complex changes in growth rates and directions of its individual cells. Cell growth, which is driven by turgor pressure, largely depends on the cell walls, which allow cell expansion through synthesis and structural changes. A previous study revealed a major contribution of wall isotropy in organ emergence, through the disorganization of cortical microtubules. We show here that this disorganization is coupled with the transcriptional control of genes involved in wall remodelling. Some of these genes are induced when microtubules are disorganized and cells shift to isotropic growth. Mechanical modelling shows that this coupling has the potential to compensate for reduced cell expansion rates induced by the shift to isotropic growth. Reciprocally, cell wall loosening induced by different treatments or altered cell wall composition promotes a disruption of microtubule alignment. Our data thus indicate the existence of a regulatory module activated during organ outgrowth, linking microtubule arrangements to cell wall remodelling.

Flower development: from morphodynamics to morphomechanics.

The shoot apical meristem (SAM) is a small population of stem cells that continuously generates organs and tissues. We will discuss here flower formation at the SAM, which involves a complex network of regulatory genes and signalling molecules. A major downstream target of this network is the extracellular matrix or cell wall, which is a local determinant for both growth rates and growth directions. We will discuss here a number of recent studies aimed at analysing the link between cell wall structure and molecular regulation. This has involved multidisciplinary approaches including quantitative imaging, molecular genetics, computational biology and biophysics. A scenario emerges where molecular networks impact on both cell wall anisotropy and synthesis, thus causing the rapid outgrowth of organs at specific locations. More specifically, this involves two interdependent processes: the activation of wall remodelling enzymes and changes in microtubule dynamics.This article is part of the themed issue 'Systems morphodynamics: understanding the development of tissue hardware'.

An auxin-mediated shift toward growth isotropy promotes organ formation at the shoot meristem in Arabidopsis.

To control morphogenesis, molecular regulatory networks have to interfere with the mechanical properties of the individual cells of developing organs and tissues, but how this is achieved is not well known. We study this issue here in the shoot meristem of higher plants, a group of undifferentiated cells where complex changes in growth rates and directions lead to the continuous formation of new organs. Here, we show that the plant hormone auxin plays an important role in this process via a dual, local effect on the extracellular matrix, the cell wall, which determines cell shape. Our study reveals that auxin not only causes a limited reduction in wall stiffness but also directly interferes with wall anisotropy via the regulation of cortical microtubule dynamics. We further show that to induce growth isotropy and organ outgrowth, auxin somehow interferes with the cortical microtubule-ordering activity of a network of proteins, including AUXIN BINDING PROTEIN 1 and KATANIN 1. Numerical simulations further indicate that the induced isotropy is sufficient to amplify the effects of the relatively minor changes in wall stiffness to promote organogenesis and the establishment of new growth axes in a robust manner.