38 research outputs found

    What remains of the evidence for auxin feedback on PIN polarity patterns?

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    In light of recent findings, the feedback between auxin and PIN that plays a major role in models for self-organized auxin patterning requires revisiting

    Evolution of networks for body plan patterning; interplay of modularity, robustness and evolvability.

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    A major goal of evolutionary developmental biology (evo-devo) is to understand how multicellular body plans of increasing complexity have evolved, and how the corresponding developmental programs are genetically encoded. It has been repeatedly argued that key to the evolution of increased body plan complexity is the modularity of the underlying developmental gene regulatory networks (GRNs). This modularity is considered essential for network robustness and evolvability. In our opinion, these ideas, appealing as they may sound, have not been sufficiently tested. Here we use computer simulations to study the evolution of GRNs' underlying body plan patterning. We select for body plan segmentation and differentiation, as these are considered to be major innovations in metazoan evolution. To allow modular networks to evolve, we independently select for segmentation and differentiation. We study both the occurrence and relation of robustness, evolvability and modularity of evolved networks. Interestingly, we observed two distinct evolutionary strategies to evolve a segmented, differentiated body plan. In the first strategy, first segments and then differentiation domains evolve (SF strategy). In the second scenario segments and domains evolve simultaneously (SS strategy). We demonstrate that under indirect selection for robustness the SF strategy becomes dominant. In addition, as a byproduct of this larger robustness, the SF strategy is also more evolvable. Finally, using a combined functional and architectural approach, we determine network modularity. We find that while SS networks generate segments and domains in an integrated manner, SF networks use largely independent modules to produce segments and domains. Surprisingly, we find that widely used, purely architectural methods for determining network modularity completely fail to establish this higher modularity of SF networks. Finally, we observe that, as a free side effect of evolving segmentation and differentiation in combination, we obtained in-silico developmental mechanisms resembling mechanisms used in vertebrate development

    Periodic lateral root priming : What makes it tick?

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    Conditioning small groups of root pericycle cells for future lateral root formation has a major impact on overall plant root architecture. This priming of lateral roots occurs rhythmically, involving temporal oscillations in auxin response in the root tip. During growth, this process generates a spatial pattern of prebranch sites, an early stage in lateral root formation characterized by a stably maintained high auxin response. To date, the molecular mechanism behind this rhythmicity has remained elusive. Some data implicate a cell-autonomous oscillation in gene expression, while others strongly support the importance of tissue-level modulations in auxin fluxes. Here, we summarize the experimental data on periodic lateral root priming. We present a theoretical framework that distinguishes between a priming signal and its subsequent memorization and show how major roles for auxin fluxes and gene expression naturally emerge from this framework. We then discuss three mechanisms that could potentially induce oscillations of auxin response: cell-autonomous oscillations, Turing-type patterning, and tissue-level oscillations in auxin fluxes, along with specific properties of lateral root priming that may be used to discern which type of mechanism is most likely to drive lateral root patterning. We conclude with suggestions for future experiments and modeling studies

    Periodic lateral root priming : What makes it tick?

    No full text
    Conditioning small groups of root pericycle cells for future lateral root formation has a major impact on overall plant root architecture. This priming of lateral roots occurs rhythmically, involving temporal oscillations in auxin response in the root tip. During growth, this process generates a spatial pattern of prebranch sites, an early stage in lateral root formation characterized by a stably maintained high auxin response. To date, the molecular mechanism behind this rhythmicity has remained elusive. Some data implicate a cell-autonomous oscillation in gene expression, while others strongly support the importance of tissue-level modulations in auxin fluxes. Here, we summarize the experimental data on periodic lateral root priming. We present a theoretical framework that distinguishes between a priming signal and its subsequent memorization and show how major roles for auxin fluxes and gene expression naturally emerge from this framework. We then discuss three mechanisms that could potentially induce oscillations of auxin response: cell-autonomous oscillations, Turing-type patterning, and tissue-level oscillations in auxin fluxes, along with specific properties of lateral root priming that may be used to discern which type of mechanism is most likely to drive lateral root patterning. We conclude with suggestions for future experiments and modeling studies

    Periodic Lateral Root Priming: What Makes It Tick?

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    Quantitative plant biologyβ€”Old and new

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    Quantitative approaches in plant biology have a long history that have led to several ground-breaking discoveries and given rise to new principles, new paradigms and new methodologies. We take a short historical trip into the past to explore some of the many great scientists and influences that have led to the development of quantitative plant biology. We have not been constrained by historical fact, although we have tried not to deviate too much. We end with a forward look, expressing our hopes and ambitions for this exciting interdisciplinary field

    Bootstrapping and pinning down the root meristem; the auxin-PLT-ARR network unites robustness and sensitivity in meristem growth control

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    After germination, the meristem of the embryonic plant root becomes activated, expands in size and subsequently stabilizes to support post-embryonic root growth. The plant hormones auxin and cytokinin, together with master transcription factors of the PLETHORA (PLT) family have been shown to form a regulatory network that governs the patterning of this root meristem. Still, which functional constraints contributed to shaping the dynamics and architecture of this network, has largely remained unanswered. Using a combination of modeling approaches we reveal how the interplay between auxin and PLTs enables meristem activation in response to above-threshold stimulation, while its embedding in a PIN-mediated auxin reflux loop ensures localized PLT transcription and thereby, a finite meristem size. We furthermore demonstrate how this constrained PLT transcriptional domain enables independent control of meristem size and division rates, further supporting a division of labor between auxin and PLT. We subsequently reveal how the weaker auxin antagonism of the earlier active Arabidopsis response regulator 12 (ARR12) may arise from the absence of a DELLA protein interaction domain. Our model indicates that this reduced strength is essential to prevent collapse in the early stages of meristem expansion while at later stages the enhanced strength of Arabidopsis response regulator 1 (ARR1) is required for sufficient meristem size control. Summarizing, our work indicates that functional constraints significantly contribute to shaping the auxin-cytokinin-PLT regulatory network

    Auxin information processing : partners and interactions beyond the usual suspects

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    Auxin plays a major role in a variety of processes involved in plant developmental patterning and its adaptation to environmental conditions. Therefore, an important question is how specificity in auxin signalling is achieved, that is, how a single signalling molecule can carry so many different types of information. In recent years, many studies on auxin specificity have been published, unravelling increasingly more details on differential auxin sensitivity, expression domains and downstream partners of the auxin receptors (transport inhibitor response 1 (TIR1) and other auxin signaling F-box proteins (AFB)), transcriptional repressors that are degraded in response to auxin (AUX/IAA) and downstream auxin response factors (ARF) that together constitute the plant’s major auxin response pathways. These data are critical to explain how, in the same cells, different auxin levels may trigger different responses, as well as how in different spatial or temporal contexts similar auxin signals converge to different responses. However, these insights do not yet answer more complex questions regarding auxin specificity. As an example, they leave open the question of how similar sized auxin changes at similar locations result in different responses depending on the duration and spatial extent of the fluctuation in auxin levels. Similarly, it leaves unanswered how, in the case of certain tropisms, small differences in signal strength at both sides of a plant organ are converted into an instructive auxin asymmetry that enables a robust tropic response. Finally, it does not explain how, in certain cases, substantially different auxin levels become translated into similar cellular responses, while in other cases similar auxin levels, even when combined with similar auxin response machinery, may trigger different responses. In this review, we illustrate how considering the regulatory networks and contexts in which auxin signalling takes place helps answer these types of fundamental questions

    Auxin information processing : partners and interactions beyond the usual suspects

    No full text
    Auxin plays a major role in a variety of processes involved in plant developmental patterning and its adaptation to environmental conditions. Therefore, an important question is how specificity in auxin signalling is achieved, that is, how a single signalling molecule can carry so many different types of information. In recent years, many studies on auxin specificity have been published, unravelling increasingly more details on differential auxin sensitivity, expression domains and downstream partners of the auxin receptors (transport inhibitor response 1 (TIR1) and other auxin signaling F-box proteins (AFB)), transcriptional repressors that are degraded in response to auxin (AUX/IAA) and downstream auxin response factors (ARF) that together constitute the plant’s major auxin response pathways. These data are critical to explain how, in the same cells, different auxin levels may trigger different responses, as well as how in different spatial or temporal contexts similar auxin signals converge to different responses. However, these insights do not yet answer more complex questions regarding auxin specificity. As an example, they leave open the question of how similar sized auxin changes at similar locations result in different responses depending on the duration and spatial extent of the fluctuation in auxin levels. Similarly, it leaves unanswered how, in the case of certain tropisms, small differences in signal strength at both sides of a plant organ are converted into an instructive auxin asymmetry that enables a robust tropic response. Finally, it does not explain how, in certain cases, substantially different auxin levels become translated into similar cellular responses, while in other cases similar auxin levels, even when combined with similar auxin response machinery, may trigger different responses. In this review, we illustrate how considering the regulatory networks and contexts in which auxin signalling takes place helps answer these types of fundamental questions
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