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<!DOCTYPE html PUBLIC "-//W3C//DTD HTML 4.0 Transitional//EN">
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<title>Spatiotemporal Model of the Asymmetric Division Cycle of <em>Caulobacter</em> cell</title>
<meta name="Description" content="content="A" mathematical="" model="" of="" cell="" cycle="" control="" in="" caulobacter"="">
<meta name="keywords" content="mathematical model Caulobacter model cell cycle control Caulobacter crescentus computational biology systems biology modeling biological network CtrA GcrA DnaA Caulobacter mutants">
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<div id="top"><h1>Spatiotemporal Model of the Asymmetric Division Cycle of <em>Caulobacter</em> Cell</h1></div>
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<h3>1. DivJ-dependent phosphorylation of DivK is crucial for switching PleC from a phosphatase to a kinase</h3>
<p align="center"><img "="" src="./CCGraph/23.png" width="60%"></p>
<p class="style1" align="center"> Figure 2.4: <strong>DivJ initiates the PleC phosphatase-to-kinase transition. For the full model, we plot signal-response curves (one-parameter bifurcation diagrams) for the steady state levels of (A) PleC kinase, (B) DivK~P, (C) PleD~P, and (D) DivK bound to PleC as functions of total DivJ (the parameter DivJ_tot in the model). Solid lines, stable steady states; dashed lines, unstable steady states. In our model, PleC_tot = constant = 1.0, but total DivK, total CtrA, and total PleD depends on DivJ_tot.
</strong></p>
<h3>2. DivJ-dependent phosphorylation of DivK is crucial for switching PleC from a phosphatase to a kinase</h3>
<p align="center"><img "="" src="./CCGraph/24.png" width="75%"></p>
<p class="style1" align="center"> Figure 2.5: <strong>Over-expressing DivK causes a drop in PleD phosphorylation.
The steady state level of PleD~P is plotted against increasing amount of total DivK for (A) Δ<em>divJ divK</em><sub>D53N</sub>, (B) Δ<em>divJ</em>, and (C) wild type background. Although the absolute levels vary among the three cell types, in each case PleD~P level shows an initial increase followed by a drop at high DivK.
</strong></p>
<p align="center"><img "="" src="./CCGraph/25.png" width="60%"></p>
<p class="style1" align="center"> Figure 2.6: <strong>Over-expressing DivK causes activation the PleC switch independent of DivJ. (A) Two-parameter bifurcation diagram, indicating how the PleC switch behaves in cells expressing different levels of DivJ_tot and DivK_total (<em>k</em><sub>syn_dk</sub> is the rate constant for synthesis of DivK). PleC exhibits bistability within the crescent-shaped region bounded by the blue lines. (B) One-parameter bifurcation diagrams (signal-response curves) for three different values of <em>k</em><sub>syn_dk</sub>, indicated by the dashed hoizontal lines in panel A. Notice that PleC kinase level is always low if <em>k</em><sub>syn_dk</sub><0.011 and always high if <em>k</em><sub>syn_dk</sub>>0.082.
</strong></p>
<h3>3. The PleC-DivJ-DivK switch confers bistability to the DivL-CckA-CtrA module</h3>
<p align="center"><img "="" src="./CCGraph/26.png" width="60%"></p>
<p class="style1" align="center"> Figure 2.7: <strong>The DivJ-PleC-DivK module controls the DivL-CckA-CtrA module.
When the PleC switch is activated, DivK~P binds to DivL and inactivates components of the CckA module. One parameter bifurcation diagrams show the steady state levels of (A) DivL, (B) CckA kinase, (C) CtrA~P, and (D) CpdR~P as functions of DivJ_tot.
</strong></p>
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