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Monk, N. A. M.

Publications and source records attributed to Monk, N. A. M..

3 recordsLinked to original sources

Implementing a framework of carbon and nitrogen feedback responses into a plant resource allocation model

O_LIThe allocation of resources to roots and shoots can greatly alter total plant mass. Allocation is thought to be the consequence of growth processes (i.e uptake rates, transport rates, growth rates) and the communication between them via signalling mechanisms. Feedbacks that alter growth processes are induced in nature by changes in the internal pools of carbon and nitrogen, but how these function together to define allocation remains unclear. C_LIO_LIWe introduce a framework model of internal feedback responses to changes in plant carbon and nitrogen concentrations. We evaluate how well the model responds to changes in carbon and nitrogen availability by simulating external environmental perturbations that influence the uptake of resources. C_LIO_LIThe model reflects experimental results when looking at the effect of atmospheric CO2 and soil nitrogen concentrations on total plant mass and replicates observed responses to leaf defoliation events. Overall this shows that a combination of known signalling mechanisms are sufficient to reproduce experimentally observed responses to external resource availability. C_LIO_LIModel simulations highlight key areas of uncertainty where more empirical data is needed. In particular, quantitative data is needed to establish the strengths and rates at which feedback responses to carbon and nitrogen substrate concentrations alter growth and uptake rates. C_LI

plant biology↗

Perturbation analysis of a multi-morphogen Turing Reaction-Diffusion stripe patterning system reveals key regulatory interactions

Periodic patterning is extremely widespread in developmental biology and is broadly modelled by Reaction-Diffusion (RD) processes. However, the minimal two-component RD system is vastly simpler than the multimolecular events that current biology is now able to describe. Moreover, RD models are typically underconstrained such that it is often hard to meaningfully relate the model architecture to real interactions measured experimentally. To address both these issues, we investigated the periodic striped patterning of the rugae (transverse ridges) in the roof of the mammalian palate. We experimentally implicated a small number of major signalling pathways and established theoretical limits on the number of pathway network topologies that can account for the stable spatial phase relationships of their observed signalling outputs. We further conducted perturbation analysis both experimentally and in silico, critically to assess the effects of perturbations on established patterns. We arrived at a relatively highly-constrained number of possible networks and found that these share some common motifs. Finally, we examined the dynamics of pattern appearance and discovered a core network consisting of epithelium-specific FGF and Wnt as mutually antagonistic "activators" and Shh as the "inhibitor", which initiates the periodicity and whose existence constrains the network topology still further. Together these studies articulate the principles of multi-morphogen RD patterning and demonstrate the utility of perturbation analysis as a tool for constraining networks in this and, in principle, any RD system.

developmental biology↗

Anteroposterior patterning of the zebrafish ear through Fgf- and Hh-dependent regulation of hmx3a expression

In the zebrafish, Fgf and Hh signalling assign anterior and posterior identity, respectively, to the poles of the developing ear. Mis-expression of fgf3 or inhibition of Hh signalling results in double-anterior ears, including ectopic expression of hmx3a. To understand how this double-anterior pattern is established, we characterised transcriptional responses in Fgf gain-of-signalling or Hh loss-of-signalling backgrounds. Mis-expression of fgf3 resulted in rapid expansion of anterior otic markers, refining over time to give the duplicated pattern. Response to Hh inhibition was very different: initial anteroposterior asymmetry was retained, with de novo duplicate expression domains appearing later. We show that Hmx3a is required for normal anterior otic patterning, but neither loss nor gain of hmx3a function was sufficient to generate ear duplications. Using our data to infer a transcriptional regulatory network required for acquisition of otic anterior identity, we can recapitulate both the wild-type and the double-anterior pattern in a mathematical model.

developmental biology↗