Essential Role of Extrinsic Noise in Models of E. coli Division Control
Mattia Corigliano, Kuheli Biswas, Matteo Bocchiola, Daniele Montagnani, Ariel Amir + 1 more
TLDR
This paper introduces a unified analytical model demonstrating the essential role of extrinsic noise and molecular mechanisms in E. coli cell division.
Key contributions
- Developed a stochastic threshold-accumulation model integrating intrinsic/extrinsic noise and molecular parameters.
- Revealed a continuum of division strategies (timer to sizer), moving beyond the simple "adder" model.
- Showed extrinsic noise and specific mechanisms are crucial to match observed E. coli size fluctuations.
- Demonstrated the "adder" strategy emerges from a balance between threshold correlations and protein reset.
Why it matters
This research provides a crucial analytical framework to understand bacterial cell division at a molecular level, moving beyond phenomenological models. It highlights the often-overlooked role of extrinsic noise and specific molecular interactions in shaping diverse division strategies and size control. This framework can be applied to more complex bacterial cell-cycle models.
Original Abstract
Our understanding of cell division control in bacteria still relies largely on interpreting correlations between phenomenological variables, with limited connection to the underlying molecular mechanisms. Here, we analytically solve a stochastic threshold-accumulation model in which a size-dependent divisor protein triggers division upon reaching a noisy, autocorrelated threshold, quantifying within a unified framework the combined effects of intrinsic and extrinsic noise and key mechanistic parameters such as protein reset and threshold memory. We show that incorporating these elements yields behavior far richer than the commonly assumed adder, spanning a continuum of division strategies from timer to sizer while modulating size fluctuations in a nontrivial fashion. Comparison with single-cell E. coli data shows that extrinsic noise and additional mechanistic ingredients are required to account for the observed size fluctuations. The adder emerges when threshold correlations balance protein reset, generalizing the hypothesis that full reset is necessary to maintain adder control. Our results establish a unified analytical framework linking stochastic molecular processes to emergent division laws, to be used in more complex bacterial cell-cycle models.
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