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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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<li><a href="././index.html.html">Home</a></li>
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<h3>1. The model is able to reproduce the wild type distribution of ParA, <em>parS</em>/ParB, PopZ and FtsZ.</h3>
<p align="center"><img "="" src="./CCGraph/63.png" width="60%"></p>
<p class="style1" align="center"> Figure 5.3: <strong>Spatiotemporal distribution of ParA (right panel) and <em>parS</em>/ParB chromosome fronts in wild-type and mutant cells. Colors indicate concentration gradients from minimum (blue) to maximum (red). (A) Wild type, (B) ΔtipN, and (C) ParA overexpression. (D) parA<sub>D44A</sub> mutants express ParA<sub>D44A</sub> proteins that cannot be hydrolyzed by ParB. (E) parA<sub>G16V</sub> mutants express ParA<sub>G16V</sub> proteins that cannot form dimers. (F) parA<sub>R195E</sub> mutants express ParA<sub>R195E</sub> proteins that cannot bind DNA.
</strong></p>
<h3>2. The model reproduces delays in chromosome segregation and FtsZ mid-cell localization in ΔtipN and ParA overexpression background</h3>
<p align="center"><img "="" src="./CCGraph/64.png" width="60%"></p>
<p class="style1" align="center"> Figure 5.4: <strong>Spatiotemporal distribution of FtsZ (left panel) and PopZ (right panel) in wild-type and mutant cells. Colors indicate concentration gradients from minimum (blue) to maximum (red). (A) Wild type, (B) ΔtipN, and (C) ParA overexpression. (D) parA<sub>D44A</sub> mutants express ParA<sub>D44A</sub> proteins that cannot be hydrolyzed by ParB. (E) parA<sub>G16V</sub> mutants express ParA<sub>G16V</sub> proteins that cannot form dimers. (F) parA<sub>R195E</sub> mutants express ParAR195E proteins that cannot bind DNA.
</strong></p>
<h3>3. The model reproduces aberrant localization of ParA mutants. PopZ may regulate chromosome segregation via binding ParA dimers instead of ParA monomers.</h3>
<p align="center"><img "="" src="./CCGraph/65.png" width="80%"></p>
<p class="style1" align="center"> Figure 5.5: <strong>Centromere segregation requires PopZ to interact with the dimeric form of ParA. Colors indicate concentration gradients from minimum (blue) to maximum (red). The time taken for translocating the <em>parS</em>/ParB chromosome front (upper panel), and the ParA distribution profile (lower panel) are comparable between simulations of the (A) wild type strain, and (B) a mutant strain containing a PopZ variant that cannot bind ParA monomer (popZ-SP1). (C) Simulations of a strain containing a PopZ variant that cannot bind ParA dimers (popZ-SP2) shows that the <em>parS</em>/ParB segregation is delayed.
</strong></p>
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<span style="float:right">Page designed Oct 6, 2014</span><span style="float:left">Site Design by <a class="credits" style="font-weight:800"> © Tyson's Lab</a></span><center><a class="credits" style="font-weight:800" href="mailto:cmhshirl@vt.edu"><img border="0" src="./CCGraph/mailto.gif"> webmaster</a></center>
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