Swimming of a rigid phoretic particle in an isotropic fluid is studied numerically as a function of the dimensionless solute emission rate (or Péclet number Pe). The particle sets into motion at a critical Pe. Whereas the particle trajectory is straight at small enough Pe, it is found that it looses its stability at a critical Pe in favor of a meandering motion. When Pe is increased further the particle meanders at short scale but its trajectory wraps into a circle at larger scale. Increasing even further Pe causes the swimmer to escape momentarily the circular trajectory in favor of chaotic motion lasting for a certain time, before regaining a circular trajectory, and so on. The chaotic bursts become more and more frequent as Pe increases, until the trajectory becomes fully chaotic, via intermittency scenario. The statistics of the trajectory is found to be of run and tumble-like nature at short enough time, and of diffusive nature at long time without any source of noise.

Many eukaryotic cells undergo frequent shape changes (described as amoeboid motion) that enable them to move forward. We investigate the effect of confinement on a minimal model of amoeboid swimmer. A complex picture emerges: (i) The swimmer's nature (i.e., either pusher or puller) can be modified by confinement, thus suggesting that this is not an intrinsic property of the swimmer. This swimming nature transition stems from intricate internal degrees of freedom of membrane deformation. (ii) The swimming speed might increase with increasing confinement before decreasing again for stronger confinements. (iii) A straight amoeoboid swimmer's trajectory in the channel can become unstable, and ample lateral excursions of the swimmer prevail. This happens for both pusher- and puller-type swimmers. For weak confinement, these excursions are symmetric, while they become asymmetric at stronger confinement, whereby the swimmer is located closer to one of the two walls. In this study, we combine numerical and theoretical analyses.

Several micro-organisms, such as bacteria, algae, or spermatozoa, use flagellar or ciliary activity to swim in a fluid, while many other micro-organisms instead use ample shape deformation, described as amoeboid, to propel themselves by either crawling on a substrate or swimming. Many eukaryotic cells were believed to require an underlying substratum to migrate (crawl) by using membrane deformation (like blebbing or generation of lamellipodia) but there is now increasing evidence that a large variety of cells (including those of the immune system) can migrate without the assistance of focal adhesion, allowing them to swim as efficiently as they can crawl. This paper details the analysis of amoeboid swimming in a confined fluid by modeling the swimmer as an inextensible membrane deploying local active forces (with zero total force and torque). The swimmer displays a rich behavior: it may settle into a straight trajectory in the channel or navigate from one wall to the other depending on its confinement. The nature of the swimmer is also found to be affected by confinement: the swimmer can behave, on the average over one swimming cycle, as a pusher at low confinement, and becomes a puller at higher confinement, or vice versa. The swimmer's nature is thus not an intrinsic property. The scaling of the swimmer velocity V with the force amplitude A is analyzed in detail showing that at small enough A, V ∼ A 2 /η 2 (where η is the viscosity of the ambient fluid), whereas at large enough A, V is independent of the force and is determined solely by the stroke cycle frequency and swimmer size. This finding starkly contrasts with currently known results found from swimming models where motion is based on ciliary and flagellar activity, where V ∼ A/η. To conclude, two definitions of efficiency as put forward in the literature are analyzed with distinct outcomes. We find that one type of efficiency has an optimum as a function of confinement while the other does not. Future perspectives are outlined.

No abstract

No abstract

The motion of an autophoretic spherical particle in a simple fluid is analyzed. This motion is powered by a chemical species which is absorbed/emitted by the particle and which diffuses and is advected in the surrounding fluid. The transition from the nonmotile to the motile state occurs if the Péclet number P e (defined as the ratio of the solute emission rate over the solute diffusion rate) is sufficiently large. We first analyze the axisymmetric case (restricting the particle to a unique direction). In this case, we find that the motion of the particle transits from a motionless to a directed motion at a given critical P e. Increasing P e, we find a second critical value where the particle becomes stagnant in a symmetric flow. Further increase of P e leads to a recovery of motile motion. When P e is increased even further, the particle shows a periodic motion undergoing a subharmonic cascade before entering chaos. In this regime, the mean square displacement behaves quadratically with time (a ballistic regime). When the axisymmetry constraint is relaxed, allowing the particle to freely move in three-dimensional space, we find that at a small P e the particle moves in a straight manner. There exists a critical value where the particle exhibits an oscillatory motion with a meandering trajectory. Increasing further P e leads to chaotic bursts for some time, before entering fully into chaos via intermittency scenario at a critical P e number. In this regime, the particle shows run and tumble like dynamics: the trajectory is then characterized by a ballistic swimming nature at a short time and a diffusive nature at a long time.

No abstract

The viral infection process is a battle between host defense response and pathogen antagonizing action. Several studies have established a tight link between the viral RNA silencing suppressor (RSS) and the repression of salicylic acid (SA)-mediated defense responses, nonetheless host factors directly linking an RSS and the SA pathway remains unidentified. From yeast two-hybrid analysis, we identified an interaction between the potyviral RSS helper-component proteinase (HCPro) and SA-binding protein SABP3. Co-localization and bimolecular fluorescence complementation analyses validated the direct in vivo interaction between Turnip mosaic virus (TuMV) HCPro and the Arabidopsis homologue of SABP3, AtCA1. Additionally, transient expression of TuMV HCPro demonstrated its ability to act as a negative regulator of AtCA1. When the plants of the AtCA1 knockout mutant line were inoculated with TuMV, our results indicated that AtCA1 is essential to restrict viral spreading and accumulation, induce SA accumulation, and trigger the SA pathway. Unexpectedly, the AtCA1 overexpression line also displayed a similar phenotype, suggesting that the constitutive expression of AtCA1 antagonizes the SA pathway. Taken together, our results depict AtCA1 as an essential regulator of SA defense responses. Moreover, the interaction of potyviral HCPro with this regulator compromises the SA pathway to weaken host defense responses and facilitate viral infection.