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Two-site or cooperative binding models did not substantially improve the fits.
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However, this could not be examined further, as a two-compartment reversible binding model did not give stable parameter estimates.
The diffusion-binding model did not lead to directional motion, indicating that diffusion of the ParB/ parS complex coupled with its biochemical interplay with DNA-bound ParA-ATP dimers does not create a Brownian ratchet.
Moreover, the diffusion-binding model did not work better than a simple diffusion model ('Materials and methods') in which the partition complex diffuses without interacting with ParA-ATP dimers.
As shown in Figure 4B and 4C, this diffusion-binding model does not lead to fast or robust segregation.
This can be seen in Video 2. As a result, the diffusion-binding model does not perform better than the model in which the partition complex only passively diffuses (no interaction with ParA-ATP dimers).
The models did not seem particularly rattled.
The trained SVR models do not directly predict PFMs, but the similarity of the DNA-binding specificities of two TFs.
However these models do not inform whether the accessibility is a prerequisite or a secondary effect of p63 binding.
This model did not converge.
What models don't scale?
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