Studying root-environment interactions in structured microdevices.

When interacting with the environment, plant roots integrate sensory information over space and time in order to respond appropriately under non-uniform conditions. The complexity and dynamic properties of soil across spatial and temporal scales pose a significant technical challenge for research into the mechanisms that drive metabolism, growth, and development in roots, as well as on inter-organismal networks in the rhizosphere. Synthetic environments, combining microscopic access and manipulation capabilities with soil-like heterogeneity, are needed to elucidate the intriguing antagonism that characterizes subsurface ecosystems. Microdevices have provided opportunities for innovative approaches to observe, analyse, and manipulate plant roots and advanced our understanding of their development, physiology, and interactions with the environment. Initially conceived as perfusion platforms for root cultivation under hydroponic conditions, microdevice design has, in recent years, increasingly shifted to better reflect the complex growth conditions in soil. Heterogeneous micro-environments have been created through co-cultivation with microbes, laminar flow-based local stimulation, and physical obstacles and constraints. As such, structured microdevices provide an experimental entry point into the complex network behaviour of soil communities.

Filament flexibility enhances power transduction of F-actin bundles.

The dynamic behavior of bundles of actin filaments growing against a loaded obstacle is investigated through a generalized version of the standard multifilament Brownian Ratchet model in which the (de)polymerizing filaments are treated not as rigid rods but as semiflexible discrete wormlike chains with a realistic value of the persistence length. By stochastic dynamic simulations, we study the relaxation of a bundle of Nf filaments with a staggered seed arrangement against a harmonic trap load in supercritical conditions. Thanks to the time scale separation between the wall motion and the filament size relaxation, mimicking realistic conditions, this setup allows us to extract a full load-velocity curve from a single experiment over the trap force/size range explored. We observe a systematic evolution of steady nonequilibrium states over three regimes of bundle lengths L. A first threshold length Λ marks the transition between the rigid dynamic regime (L < Λ), characterized by the usual rigid filament load-velocity relationship V(F), and the flexible dynamic regime (L > Λ), where the velocity V(F, L) is an increasing function of the bundle length L at a fixed load F, the enhancement being the result of an improved level of work sharing among the filaments induced by flexibility. A second critical length corresponds to the beginning of an unstable regime characterized by a high probability to develop escaping filaments which start growing laterally and thus do not participate anymore in the generation of the polymerization force. This phenomenon prevents the bundle from reaching at this critical length the limit behavior corresponding to perfect load sharing.

On the properties of a bundle of flexible actin filaments in an optical trap.

We establish the statistical mechanics framework for a bundle of Nf living and uncrosslinked actin filaments in a supercritical solution of free monomers pressing against a mobile wall. The filaments are anchored normally to a fixed planar surface at one of their ends and, because of their limited flexibility, they grow almost parallel to each other. Their growing ends hit a moving obstacle, depicted as a second planar wall, parallel to the previous one and subjected to a harmonic compressive force. The force constant is denoted as the trap strength while the distance between the two walls as the trap length to make contact with the experimental optical trap apparatus. For an ideal solution of reactive filaments and free monomers at fixed free monomer chemical potential µ1, we obtain the general expression for the grand potential from which we derive averages and distributions of relevant physical quantities, namely, the obstacle position, the bundle polymerization force, and the number of filaments in direct contact with the wall. The grafted living filaments are modeled as discrete Wormlike chains, with F-actin persistence length ℓp, subject to discrete contour length variations ±d (the monomer size) to model single monomer (de)polymerization steps. Rigid filaments (ℓp = ∞), either isolated or in bundles, all provide average values of the stalling force in agreement with Hill's predictions Fs (H)=NfkBTln(ρ1/ρ1c)/d, independent of the average trap length. Here ρ1 is the density of free monomers in the solution and ρ1c its critical value at which the filament does not grow nor shrink in the absence of external forces. Flexible filaments (ℓp < ∞) instead, for values of the trap strength suitable to prevent their lateral escape, provide an average bundle force and an average trap length slightly larger than the corresponding rigid cases (few percents). Still the stalling force remains nearly independent on the average trap length, but results from the product of two strongly L-dependent contributions: the fraction of touching filaments ∝〈L〉(O.T.) (2) and the single filament buckling force ∝〈L〉(O.T.) (-2).

Autoimmune diseases and celiac disease which came first: genotype or gluten?

Celiac disease (CD) is associated with several autoimmune diseases (ADs) and, in particular, thyroid autoimmunity (TA) and Type 1 diabetes (T1D). TA and T1D are defined as 'associated conditions' to CD (conditions at increased prevalence in CD but not directly related to gluten ingestion). The diagnosis of CD may precede or follow that of TA/T1D. To date, the available evidence suggests that the common genetic background is the main factor determining the high prevalence of the association. Conversely, no conclusive findings clarify whether extrinsic gluten-related factors (age at the first introduction, concomitant breastfeeding, length of gluten exposure and gluten-free diet) may link CD to the ADs. The aim of this review is to evaluate whether genetic background alone could explain the association between CD and ADs or if gluten-related factors ought to be considered. The pathophysiological links clarifying how the gluten-related factors could predispose to ADs will also be discussed.