14 research outputs found
Noise and Robustness in Phyllotaxis
A striking feature of vascular plants is the regular arrangement of lateral organs on the stem, known as phyllotaxis. The most common phyllotactic patterns can be described using spirals, numbers from the Fibonacci sequence and the golden angle. This rich mathematical structure, along with the experimental reproduction of phyllotactic spirals in physical systems, has led to a view of phyllotaxis focusing on regularity. However all organisms are affected by natural stochastic variability, raising questions about the effect of this variability on phyllotaxis and the achievement of such regular patterns. Here we address these questions theoretically using a dynamical system of interacting sources of inhibitory field. Previous work has shown that phyllotaxis can emerge deterministically from the self-organization of such sources and that inhibition is primarily mediated by the depletion of the plant hormone auxin through polarized transport. We incorporated stochasticity in the model and found three main classes of defects in spiral phyllotaxis â the reversal of the handedness of spirals, the concomitant initiation of organs and the occurrence of distichous angles â and we investigated whether a secondary inhibitory field filters out defects. Our results are consistent with available experimental data and yield a prediction of the main source of stochasticity during organogenesis. Our model can be related to cellular parameters and thus provides a framework for the analysis of phyllotactic mutants at both cellular and tissular levels. We propose that secondary fields associated with organogenesis, such as other biochemical signals or mechanical forces, are important for the robustness of phyllotaxis. More generally, our work sheds light on how a target pattern can be achieved within a noisy background
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Research data supporting Cell size and growth regulation in the Arabidopsis thaliana apical stem cell niche
Confocal membrane data, segmentation data, and cell lineage information for cells in the shoot apical meristem of 6 NPA-treated Arabidopsis plants
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Cell size and growth regulation in the apical stem cell niche
Cell size and growth kinetics are fundamental cellular properties with important physiological implications. Classical studies on yeast, and recently on bacteria, have identified rules for cell size regulation in single cells, but in the more complex environment of multicellular tissues, data have been lacking. In this study, to characterize cell size and growth regulation in a multicellular context, we developed a 4D imaging pipeline and applied it to track and quantify epidermal cells over 3-4 d in shoot apical meristems. We found that a cell size checkpoint is not the trigger for G2/M or cytokinesis, refuting the unexamined assumption that meristematic cells trigger cell cycle phases upon reaching a critical size. Our data also rule out models in which cells undergo G2/M at a fixed time after birth, or by adding a critical size increment between G2/M transitions. Rather, cell size regulation was intermediate between the critical size and critical increment paradigms, meaning that cell size fluctuations decay by âŒ75% in one generation compared with 100% (critical size) and 50% (critical increment). Notably, this behavior was independent of local cell-cell contact topologies and of position within the tissue. Cells grew exponentially throughout the first >80% of the cell cycle, but following an asymmetrical division, the small daughter grew at a faster exponential rate than the large daughter, an observation that potentially challenges present models of growth regulation. These growth and division behaviors place strong constraints on quantitative mechanistic descriptions of the cell cycle and growth control.This work was supported by the Gatsby Charitable Foundation through Grant GAT3395-PR4 (to H.J.) and Fellowships GAT3272/C and GAT3273-PR1 (to E.M.M.), Swedish Research Council Grant VR2013:4632 and Knut and Alice Wallenberg Foundation Grant KAW2012.0050 (to H.J.), the Howard Hughes Medical Institute and Gordon and Betty Moore Foundation Grant GBMF3406 (to E.M.M.), and National Science Foundation Faculty Early Career Development (CAREER) Program Award MCB-1149328 (to K.C.H.)
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Fluctuations of the transcription factor ATML1 generate the pattern of giant cells in the sepal
Multicellular development produces patterns of specialized cell types. Yet, it is often unclear how individual cells within a field of identical cells initiate the patterning process. Using live imaging, quantitative image analyses and modeling, we show that during sepal development, fluctuations in the concentration of the transcription factor ATML1 pattern a field of identical epidermal cells to differentiate into giant cells interspersed between smaller cells. We find that ATML1 is expressed in all epidermal cells. However, its level fluctuates in each of these cells. If ATML1 levels surpass a threshold during the G2 phase of the cell cycle, the cell will likely enter a state of endoreduplication and become giant. Otherwise, the cell divides. Our results demonstrate a fluctuation-driven patterning mechanism for how cell fate decisions can be initiated through a random yet tightly regulated process.This work was supported by NSF IOS Plant, Fungal, and Microbial Developmental Mechanisms grants IOS-1256733 and IOS-1553030 (AKHR). This work was further supported by the Gatsby Charitable Foundation (GAT3272/GLC to JL and GAT3395/PR4 to HJ) and the Swedish Research Council (VR2013:4632 to HJ). JT and PFJ acknowledge postdoctoral fellowships provided by the Herchel Smith Foundation. This work made use of the Cornell Center for Materials Research Shared Facilities, which are supported through the NSF MRSEC program (DMR-1120296)