A Self-Controlled and Self-Healing Model of Bacterial Cells

Abstract

A new kind of self-assembly model, morphogenetic (M) systems, assembles spatial units into larger structures through local interactions of simpler components and enables discovery of new principles for cellular membrane assembly, development, and its interface function. The model is based on interactions among three kinds of constitutive objects such as tiles and protein-like elements in discrete time and continuous 3D space. It was motivated by achieving a balance between three conflicting goals: biological, physical-chemical, and computational realism. A recent example is a unified model of morphogenesis of a single biological cell, its membrane and cytoskeleton formation, and finally, its self-reproduction. Here, a family of dynamic M systems (Mbac) is described with similar characteristics, modeling the process of bacterial cell formation and division that exhibits bacterial behaviors of living cells at the macro-level (including cell growth that is self-controlled and sensitive to the presence/absence of nutrients transported through membranes), as well as self-healing properties. Remarkably, it consists of only 20 or so developmental rules. Furthermore, since the model exhibits membrane formation and septic mitosis, it affords more rigorous definitions of concepts such as injury and self-healing that enable quantitative analyses of these kinds of properties. Mbac shows that self-assembly and interactions of living organisms with their environments and membrane interfaces are critical for self-healing, and that these properties can be defined and quantified more rigorously and precisely, despite their complexity.

The Host Cytoskeleton Functions as a Pleiotropic Scaffold: Orchestrating Regulation of the Viral Life Cycle and Mediating Host Antiviral Innate Immune Responses

“…Bacterial infections and inflammation can disrupt the epithelial barrier, and host cell cytoskeletal changes in the host cell can directly mediate bacterial invasion into the intracellular environment [ 47 ]. In the intracellular niche, some bacteria then utilize the host cytoskeletal network to spread from cell to cell [ 48 ]. The binding of the Listeria monocytogenes surface proteins (InlA) to cell receptors promotes two posttranslational modifications of E-cadherin, primarily comprising host kinase Src phosphorylation followed by ubiquitination by the E3 ubiquitin ligase Hakai.…”