Although microtubule orientations and PIN protein localizations are known to mark a common apical–basal axis in the root 
, our findings in the SAM show an unexpected level of coordination between what are, in the SAM, highly dynamic subcellular markers. In the SAM, PIN1 polarities change on a time course of hours, with reversals in polarity associated with primordium formation 
. Microtubules also exhibit dynamic reorientations, especially at the meristem tip 
. That these two dynamic cellular components are highly coordinated suggests either that they are causally dependent on one another or that their localizations are both regulated by a common upstream factor. Our data strongly suggests the latter since microtubule arrangements do not depend on auxin transport for their correlated response to cell ablation even at a distance from the ablation site. Also, after microtubule depolymerization, PIN1 localization remains polarized and can shift both during primordium development and in response to ablation. If auxin gradients or flux patterns are not required for coordinating PIN1 polarities and microtubule orientations, what could act as the upstream patterning agent? Considering recent findings, it seems likely that mechanical signals coordinate their activities. For example local up-regulation of a pectin methyl esterase is sufficient to induce ectopically the full program of flower development, suggesting that changes to the mechanical properties of cell walls are sufficient to induce the usual changes to both microtubule orientations as well as PIN1 polarities 
. Also, mechanical manipulation of Arabidopsis
roots is sufficient to induce lateral root initiation, and the earliest event so far identified marking lateral root initiation is the relocalization of PIN1 protein in root protoxylem cells 
. We investigated the role of mechanical signals by inhibiting cellulose synthesis using isoxaben to alter cell wall properties. We reasoned that if the addition of load-bearing cellulose to growing cell walls was prevented, the stress levels for existing wall components should increase. Consistent with this proposal we found that isoxaben treatment induces hyperlocalization of PIN1 and an enhanced and stabilized supracellular pattern of microtubule array orientations 
. Also we found that under these circumstances PIN1 is predominantly localized to cell corners, consistent with the fact that corners and junctions are generally associated with high stresses in mechanical structures 
. Lastly, we note that isoxaben may cause distinct responses in different tissues since short-term isoxaben treatment of roots weakens rather than strengthens preexisting microtubule array alignments 
To investigate whether mechanical signals could be responsible for generating the observed patterns of PIN1 localization, we constructed a computer model that localizes PIN1 to membranes adjacent to cell walls that exhibit the highest stress. Such a model behaves similarly to previously proposed models for phyllotaxis based on differential auxin concentrations because we assume that higher auxin concentrations induce greater levels of cell wall relaxation in local cell walls compared to the cell walls of adjacent cells. Loosening of one cell wall thereby induces higher stress in the adjoining cell wall, and PIN1 becomes localized towards the cell with the most relaxed cell wall (highest auxin). Although similar to the previous chemically based models, this model is more general because wall stress depends not only on auxin but also on tissue morphology, mechanical perturbations, and the activity of any genes that modulate growth. Hence the model may explain a variety of observations in the literature that include both auxin-induced 
, mechanically induced 
, and wall-enzyme-induced changes to growth and cell polarity 
. Lastly it is worth pointing out that a possible link between mechanical stress and auxin-based patterning of phyllotaxis has been proposed previously 
. In this study it was found that coupling auxin distribution patterns to stress patterns could, under certain conditions, produce a reinforcement of the phyllotactic pattern. It will be of interest to explore such models further, in particular by enabling stress to regulate not only auxin transport patterns, but also local patterns of mechanical anisotropy, as suggested by the current study. Experimentally, it will be important to test whether cell walls play a role in locally regulating PIN1 membrane accumulation.
Independent of the particular mechanisms by which PIN1 and microtubule array orientations are regulated, their tight coupling in the SAM epidermis implies high-level coordination between growth direction, as patterned by microtubule arrays, and growth localization and gene expression, as patterned by the distribution of auxin, both during normal development and in response to wounding. An important future task will be to determine how universal this coordination is. Another will be to further investigate the role of mechanical signals in cell–cell communication in development and in coordinating growth and cell wall reinforcement with each other, and with stress.