The root meristem is shaped by brassinosteroid control of cell geometry

Growth extent and direction determine cell and whole-organ architecture. How they are spatio-temporally modulated to control size and shape is not well known. Here we tackled this question by studying the effect of brassinosteroid (BR) signalling on the structure of the root meristem. Quantification of the three-dimensional geometry of thousands of individual meristematic cells across different tissue types showed that the modulation of BR signalling yields distinct changes in growth rate and anisotropy, which affects the time that cells spend in the meristem and has a strong impact on the final root form. By contrast, the hormone effect on cell volume was minor, establishing cell volume as invariant to the effect of BR. Thus, BR has the highest effect on cell shape and growth anisotropy, regulating the overall longitudinal and radial growth of the meristem, while maintaining a coherent distribution of cell sizes. Moving from single-cell quantification to the whole organ, we developed a computational model of radial growth. The simulation demonstrates how differential BR-regulated growth between the inner and outer tissues shapes the meristem and thus explains the non-intuitive outcomes of tissue-specific perturbation of BR signalling. The combined experimental data and simulation suggest that the inner and outer tissues have distinct but coordinated roles in growth regulation.

Root meristem shaping via brassinosteroid-controlled cell geometry

Growth extent and direction determine cell and whole-organ architecture. How they are spatiotemporally modulated to control size and shape? Here we tackled this question by studying the effect of brassinosteroid (BR) signaling on the structure of the root meristem. Quantification of the 3D geometry of thousands of individual meristematic cells across different tissue types showed that modulation of BR signaling yields distinct changes in growth rate and anisotropy, which affects the time cells spend in the meristem and has a strong impact on final root form. By contrast, the hormone effect on cell volume was minor, establishing cell volume as invariant to the effect of BR. Thus, BR has highest effect on cell shape and growth anisotropy, regulating overall radial growth of the meristem, while maintaining a coherent distribution of cell sizes. Moving from single-cell quantification to the whole organ, we developed a computational model of radial growth that demonstrates how differential growth regulation by BR between the inner and outer tissues shapes the meristem. The model explains the unintuitive outcomes of tissue-specific perturbation of BR signaling and suggests that the inner and outer tissues have independent but coordinated roles in growth regulation.

Simple model of atherosclerosis in cylindrical arteries: impact of anisotropic growth on Glagov remodeling

In 1987, Seymour Glagov observed that arteries went through a two-stage remodeling process as a result of plaque growth: first, a compensatory phase where the lumen area remains approximately constant and second, an encroachment phase where the lumen area decreases over time. In this paper, we investigate the effect of growth anisotropy on Glagov remodeling in five different cases: pure radial, pure circumferential, pure axial, isotropic and general anisotropic growth where the elements of the growth tensor are chosen to minimize the total energy. We suggest that the nature of anisotropy is inclined towards the growth direction that requires the least amount of energy. Our framework is the theory of morphoelasticity on an axisymmetric arterial domain. For each case, we explore their specific effect on the Glagov curves. For the latter two cases, we also provide the changes in collagen fiber orientation and length in the intima, media and adventitia. In addition, we compare the total energy produced by growth in radial, circumferential and axial direction and deduce that using a radially dominant anisotropic growth leads to lower strain energy than isotropic growth.

Two mechanisms regulate directional cell growth in Arabidopsis lateral roots

Morphogenesis in plants depends critically on directional (anisotropic) growth. This occurs principally perpendicular to the net orientation of cellulose microfibrils (CMFs), which is in turn controlled by cortical microtubules (CMTs). In young lateral roots of Arabidopsis thaliana, growth anisotropy also depends on RAB-A5c, a plant-specific small GTPase that specifies a membrane trafficking pathway to the geometric edges of cells. Here we investigate the functional relationship between structural anisotropy at faces and RAB-A5c activity at edges during lateral root development. We show that surprisingly, inhibition of RAB-A5c function is associated with increased CMT/CMF anisotropy. We present genetic, pharmacological, and modelling evidence that this increase in CMT/CMF anisotropy partially compensates for loss of an independent RAB-A5c-mediated mechanism that maintains anisotropic growth in meristematic cells. We show that RAB-A5c associates with CMTs at cell edges, indicating that CMTs act as an integration point for both mechanisms controlling cellular growth anisotropy in lateral roots.

Arabidopsis IPGA1 is a microtubule-associated protein essential for cell expansion during petal morphogenesis

Unlike animal cells, plant cells do not possess centrosomes that serve as microtubule organizing centers; how microtubule arrays are organized throughout plant morphogenesis remains poorly understood. We report here that Arabidopsis INCREASED PETAL GROWTH ANISOTROPY 1 (IPGA1), a previously uncharacterized microtubule-associated protein, regulates petal growth and shape by affecting cortical microtubule organization. Through a genetic screen, we showed that IPGA1 loss-of-function mutants displayed a phenotype of longer and narrower petals, as well as increased anisotropic cell expansion of the petal epidermis in the late phases of flower development. Map-based cloning studies revealed that IPGA1 encodes a previously uncharacterized protein that colocalizes with and directly binds to microtubules. IPGA1 plays a negative role in the organization of cortical microtubules into parallel arrays oriented perpendicular to the axis of cell elongation, with the ipga1-1 mutant displaying increased microtubule ordering in petal abaxial epidermal cells. The IPGA1 family is conserved among land plants and its homologs may have evolved to regulate microtubule organization. Taken together, our findings identify IPGA1 as a novel microtubule-associated protein and provide significant insights into IPGA1-mediated microtubule organization and petal growth anisotropy.