ArticlePLoS computational biology2016
Mathematical Model for Length Control by the Timing of Substrate Switching in the Type III Secretion System.
Article in PLoS computational biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Robustness and the evolution of length control strategies in the T3SS and flagellar hook.Biophysical journal · 2021Article
- Crosstalk and ultrasensitivity in protein degradation pathways.PLoS computational biology · 2020Article
- On the road to structure-based development of anti-virulence therapeutics targeting the type III secretion system injectisome.MedChemComm · 2019Review
- Structural and Functional Characterization of the Type Three Secretion System (T3SS) Needle ofFrontiers in microbiology · 2019Article
- Assembly, structure, function and regulation of type III secretion systems.Nature reviews. Microbiology · 2017Review
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Authors and funding
4 authors.
Funding
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Abstract
Type III Secretion Systems (T3SS) are complex bacterial structures that provide gram-negative pathogens with a unique virulence mechanism whereby they grow a needle-like structure in order to inject bacterial effector proteins into the cytoplasm of a host cell. Numerous experiments have been performed to understand the structural details of this nanomachine during the past decade. Despite the concerted efforts of molecular and structural biologists, several crucial aspects of the assembly of this structure, such as the regulation of the length of the needle itself, remain unclear. In this work, we used a combination of mathematical and computational techniques to better understand length control based on the timing of substrate switching, which is a possible mechanism for how bacteria ensure that the T3SS needles are neither too short nor too long. In particular, we predicted the form of the needle length distribution based on this mechanism, and found excellent agreement with available experimental data from Salmonella typhimurium with only a single free parameter. Although our findings provide preliminary evidence in support of the substrate switching model, they also make a set of quantitative predictions that, if tested experimentally, would assist in efforts to unambiguously characterize the regulatory mechanisms that control the growth of this crucial virulence factor.
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