Flagellum Pumping Efficacy in Shear-Thinning Viscoelastic Fluids

Microorganism motility often takes place within complex, viscoelastic fluid environments, e.g., sperm in cervicovaginal mucus and bacteria in biofilms. In such complex fluids, strains and stresses generated by the microorganism are stored and relax across a spectrum of length and time scales and the complex fluid can be driven out of its linear response regime. Phenomena not possible in viscous media thereby arise from feedback between the "swimmer" and the complex fluid, making swimming efficiency co-dependent on the propulsion mechanism and fluid properties. Here we parameterize a flagellar motor and filament properties together with elastic relaxation and nonlinear shear-thinning properties of the fluid in a computational immersed boundary model. We then explore swimming efficiency over this parameter space. One exemplary insight is that motor efficiency (measured by the volumetric flow rate) can be boosted vs.\ degraded by moderate vs.\ strong shear-thinning of the viscoelastic environment.Comment: 15 pages, 8 figure

Multiflagellarity leads to the size-independent swimming speed of bacteria

Flagella are essential organelles of bacteria enabling their swimming motility. While monotrichous or uniflagellar bacteria possess a single flagellum at one pole of their body, peritrichous bacteria grow multiple flagella over the body surface, which form a rotating helical bundle propelling the bacteria forward. Although the adaptation of bacterial cellular features is under strong evolutionary pressure, existing evidence suggests that multiflagellarity confers no noticeable benefit to the swimming of peritrichous bacteria in bulk fluids compared with uniflagellar bacteria. This puzzling result poses a long-standing question: why does multiflagellarity emerge given the high metabolic cost of flagellar synthesis? Contrary to the prevailing wisdom that its benefit lies beyond the basic function of flagella in steady swimming, here we show that multiflagellarity provides a significant selective advantage to bacteria in terms of their swimming ability, allowing bacteria to maintain a constant swimming speed over a wide range of body size. By synergizing experiments of immense sample sizes with quantitative hydrodynamic modeling and simulations, we reveal how bacteria utilize the increasing number of flagella to regulate the flagellar motor load, which leads to faster flagellar rotation neutralizing the higher fluid drag on their larger bodies. Without such a precise balancing mechanism, the swimming speed of uniflagellar bacteria generically decreases with increasing body size. Our study sheds light on the origin of multiflagellarity, a ubiquitous cellular feature of bacteria. The uncovered difference between uniflagellar and multiflagellar swimming is important for understanding environmental influence on bacterial morphology and useful for designing artificial flagellated microswimmers.Comment: 23 pages, 4 figure

Self-propelled bacterial swimmers by helical flagella

Swimming bacteria with helical flagella are self-propelled micro-swimmers in nature, and the swimming strategies of such bacteria vary depending on the number and the position of flagella on the cell body. In this talk, we will introduce two microorganisms, multi-flagellated E. coli and single-flagellated Vibrio A. The Kirchhoff rod theory is used to model the elastic helical flagellum and the penalty method is employed to describe the dynamics of the rigid cell body. The hydrodynamic interaction between the fluid and the cell is represented by the regularized Stokes formulation. The focus of the talk will be on how bacteria reorient swimming direction.Non UBCUnreviewedAuthor affiliation: University of CincinnatiFacult

The role of myosin II in glioma invasion: A mathematical model

<div><p>Gliomas are malignant tumors that are commonly observed in primary brain cancer. Glioma cells migrate through a dense network of normal cells in microenvironment and spread long distances within brain. In this paper we present a two-dimensional multiscale model in which a glioma cell is surrounded by normal cells and its migration is controlled by cell-mechanical components in the microenvironment via the regulation of myosin II in response to chemoattractants. Our simulation results show that the myosin II plays a key role in the deformation of the cell nucleus as the glioma cell passes through the narrow intercellular space smaller than its nuclear diameter. We also demonstrate that the coordination of biochemical and mechanical components within the cell enables a glioma cell to take the mode of amoeboid migration. This study sheds lights on the understanding of glioma infiltration through the narrow intercellular spaces and may provide a potential approach for the development of anti-invasion strategies via the injection of chemoattractants for localization.</p></div

Analysis of passing time in response to microenvironmental complexity.

<p>(A,B) Initial configurations of six normal glial cells (dotted circle) and a migratory glioma cell (double circles) when the turning angles are given as <i>θ</i> = 11.3° (A) and <i>θ</i> = 21.8° (B), respectively. Here, <i>θ</i> = angle between two vectors connecting centers of two static normal glial cells: one for cells in the first and third rows, and another for cells in the first and second rows. The distance between two cells in each row is fixed. (C) Time at which a migratory glioma cell travels given distances (x-axis) under various degrees of complexities of normal cells (<i>θ</i> = 11.3° (empty circle), 16.7° (triangle), 21.8° (square)).</p

Therapeutic strategies: inhibition of tumor infiltration using blebbistatin.

<p>(A) Time courses of blebbistatin level, concentrations of bound myosin II ([<i>m</i>_<i>b</i>]), and stiffening rate of nucleus (<i>r</i>_{[<i>m</i>_<i>b</i>]}) in response to blebbistatin injection with two different doses (<i>τ</i>_<i>B</i> = 2, <i>I</i>_<i>B</i> = 1 and <i>τ</i>_<i>B</i> = 2, <i>I</i>_<i>B</i> = 5). (B) Profile of a glioma cell in the presence of blebbistatin injection with <i>τ</i>_<i>B</i> = 2, <i>I</i>_<i>B</i> = 1 (blue solid curve) and <i>τ</i>_<i>B</i> = 2, <i>I</i>_<i>B</i> = 5 (red dotted curve). The relatively low dose of blebbistatin (<i>I</i>_<i>B</i> = 1) cannot sufficiently decrease the bound myosin II level and hence the stiffening rate of the nucleus is lowered, resulting in invasion of the glioma cell through the narrow gap. When the injection strength is increased (<i>I</i>_<i>B</i> = 5), the glioma cell cannot infiltrate the narrow intercellular space between two normal cells.</p