Biology subjects

Shraiman, B. I.

Publications and source records attributed to Shraiman, B. I..

4 recordsLinked to original sources

bioRxiv2023

Epithelial flow by controlled transformation of internal force-balance geometry

Shape changes of epithelia during animal development, such as convergent extension, are achieved through concerted mechanical activity of individual cells. While much is known about the corresponding large scale tissue flow and its genetic drivers, fundamental questions regarding local control of contractile activity on cellular scale and its embryo-scale coordination remain open. To address these questions, we develop a quantitative, model-based analysis framework to relate cell geometry to local tension in recently obtained timelapse imaging data of gastrulating Drosophila embryos. This analysis provides a systematic decomposition of cell shape changes and T1-rearrangements into internally driven, active, and externally driven, passive, contributions. Our analysis provides evidence that germ band extension is driven by active T1 processes that self-organize through positive feedback acting on tensions. More generally, our findings suggest that epithelial convergent extension results from controlled transformation of internal force balance geometry which combines the effects of bottom-up local self-organization with the top-down, embryo-scale regulation by gene expression.

biophysics↗

bioRxiv2021

Visceral organ morphogenesis via calcium-patterned muscle contractions

How organs achieve their final shape is a problem at the interface between physics and developmental biology. Organs often involve multiple interacting tissue layers that must be coordinated to orchestrate the complex shape changes of development. Intense study uncovered genetic, and physical ingredients driving the form of mono layer tissue. Yet, tracing dynamics across tissue layers, and scales - from cell to tissue, to entire organs - remains an outstanding challenge. Here, we study the midgut of Drosophila embryos as a model visceral organ, to reconstruct in toto the dynamics of multi-layer organ formation in vivo. Using light-sheet microscopy, genetics, computer vision, and tissue cartography, we extract individual tissue layers to map the time course of shape across scales from cells to organ. We identify the kinematic mechanism driving the shape change due to tissue layer interactions by linking out-of-plane motion to active contraction patterns, revealing a convergent extension process in which cells deform as they flow into deepening folds. Acute perturbations of contractility in the muscle layer using non-neuronal optogenetics reveals that these contraction patterns are due to muscle activity, which induces cell shape changes in the adjacent endoderm layer. This induction cascade relies on high frequency calcium pulses in the muscle layer, under the control of hox genes. Inhibition of targets of calcium involved in myosin phosphorylation abolishes constrictions. Our study of multi-layer organogenesis reveals how genetic patterning in one layer triggers a dynamic molecular mechanism to control a physical process in the adjacent layer, to orchestrate whole-organ shape change.

developmental biology↗

bioRxiv2021

Sector search strategies for odor trail tracking

Terrestrial animals such as ants, mice and dogs often use surface-bound scent trails to establish navigation routes or to find food and mates, yet their tracking strategies are poorly understood. Tracking behavior features zig-zagging paths with animals often staying in close contact with the trail. Upon sustained loss of contact, animals execute a characteristic sequence of sweeping "casts" - wide oscillations with increasing amplitude. Here, we provide a unified description of trail-tracking behavior by introducing an optimization framework where animals search in the angular sector defined by their estimate of the trails heading and its uncertainty. In silico experiments using reinforcement learning based on this hypothesis recapitulate experimentally observed tracking patterns. We show that search geometry imposes limits on the tracking speed, and quantify its dependence on trail statistics and memory of past contacts. By formulating trail-tracking as a Bellman-type sequential optimization problem, we quantify the basic geometric elements of optimal sector search strategy, effectively explaining why and when casting is necessary. We propose a set of experiments to infer how tracking animals acquire, integrate and respond to past information on the tracked trail. More generally, we define navigational strategies relevant for animals and bio-mimetic robots, and formulate trail-tracking as a novel behavioral paradigm for learning, memory and planning.

animal behavior and cognition↗

bioRxiv2018

Phylodynamics of rapidly adapting pathogens: extinction and speciation of a Red Queen

Rapidly evolving pathogens like influenza viruses can persist by accumulating antigenic novelty fast enough to evade the adaptive immunity of the host population, yet without continuous accumulation of genetic diversity. This dynamical state is often compared to the Red Queen evolving as fast as it can just to maintain its foothold in the host population: Accumulation of antigenic novelty is balanced by the build-up of host immunity. Such Red Queen States (RQS) of continuous adaptation in large rapidly mutating populations are well understood in terms of Traveling Wave (TW) theories of population genetics. Here we shall make explicit the mapping of the established Multi-strain Susceptible-Infected-Recovered (SIR) model onto the TW theory and demonstrate that a pathogen can persist in RQS if cross-immunity is long-ranged and its population size is large populations allowing for rapid adaptation. We then investigate the stability of this state focusing on the rate of extinction and the rate of \"speciation\" defined as antigenic divergence of viral strains beyond the range of cross-inhibition. RQS states are transient, but in a certain range of evolutionary parameters can exist for the time long compared to the typical time to the most recent common ancestor (TMRCA). In this range the steady TW is unstable and the antigenic advance of the lead strains relative to the typical co-circulating viruses tends to oscillate. This results in large fluctuations in prevalence that facilitate extinction. We shall demonstrate that the rate of TW fission into antigenically uncoupled viral populations is related to fluctuations of TMRCA and construct a \"phase diagram\" identifying different regimes of viral phylodynamics as a function of evolutionary parameters.

evolutionary biology↗