Sumesh P. Thampi

Bio: Sumesh P. Thampi is an academic researcher from Indian Institute of Technology Madras. The author has contributed to research in topics: Drop (liquid) & Lattice Boltzmann methods. The author has an hindex of 21, co-authored 65 publications receiving 1983 citations. Previous affiliations of Sumesh P. Thampi include University of Oxford & Indian Institute of Technology Kanpur.

Topological defects in epithelia govern cell death and extrusion.

Abstract: Epithelial tissues (epithelia) remove excess cells through extrusion, preventing the accumulation of unnecessary or pathological cells. The extrusion process can be triggered by apoptotic signalling, oncogenic transformation and overcrowding of cells. Despite the important linkage of cell extrusion to developmental, homeostatic and pathological processes such as cancer metastasis, its underlying mechanism and connections to the intrinsic mechanics of the epithelium are largely unexplored. We approach this problem by modelling the epithelium as an active nematic liquid crystal (that has a long range directional order), and comparing numerical simulations to strain rate and stress measurements within monolayers of MDCK (Madin Darby canine kidney) cells. Here we show that apoptotic cell extrusion is provoked by singularities in cell alignments in the form of comet-shaped topological defects. We find a universal correlation between extrusion sites and positions of nematic defects in the cell orientation field in different epithelium types. The results confirm the active nematic nature of epithelia, and demonstrate that defect-induced isotropic stresses are the primary precursors of mechanotransductive responses in cells, including YAP (Yes-associated protein) transcription factor activity, caspase-3-mediated cell death, and extrusions. Importantly, the defect-driven extrusion mechanism depends on intercellular junctions, because the weakening of cell-cell interactions in an α-catenin knockdown monolayer reduces the defect size and increases both the number of defects and extrusion rates, as is also predicted by our model. We further demonstrate the ability to control extrusion hotspots by geometrically inducing defects through microcontact printing of patterned monolayers. On the basis of these results, we propose a mechanism for apoptotic cell extrusion: spontaneously formed topological defects in epithelia govern cell fate. This will be important in predicting extrusion hotspots and dynamics in vivo, with potential applications to tissue regeneration and the suppression of metastasis. Moreover, we anticipate that the analogy between the epithelium and active nematic liquid crystals will trigger further investigations of the link between cellular processes and the material properties of epithelia.

Velocity correlations in an active nematic

Abstract: The flow properties of a continuum model for an active nematic are studied and compared with recent experiments on suspensions of microtubule bundles and molecular motors. The velocity correlation length is found to be independent of the strength of the activity while the characteristic velocity scale increases monotonically as the activity is increased, both in agreement with the experimental observations. We interpret our results in terms of the creation and annihilation dynamics of a gas of topological defects.

Stabilization of active matter by flow-vortex lattices and defect ordering.

Abstract: Active systems, from bacterial suspensions to cellular monolayers, are continuously driven out of equilibrium by local injection of energy from their constituent elements and exhibit turbulent-like and chaotic patterns. Here we demonstrate both theoretically and through numerical simulations, that the crossover between wet active systems, whose behaviour is dominated by hydrodynamics, and dry active matter where any flow is screened, can be achieved by using friction as a control parameter. Moreover, we discover unexpected vortex ordering at this wet-dry crossover. We show that the self organization of vortices into lattices is accompanied by the spatial ordering of topological defects leading to active crystal-like structures. The emergence of vortex lattices, which leads to the positional ordering of topological defects, suggests potential applications in the design and control of active materials.

Defect-mediated morphologies in growing cell colonies

Abstract: Morphological trends in growing colonies of living cells are at the core of physiological and evolutionary processes. Using active gel equations, which include cell division, we show that shape changes during the growth can be regulated by the dynamics of topological defects in the orientation of cells. The friction between the dividing cells and underlying substrate drives anisotropic colony shapes toward more isotropic morphologies, by mediating the number density and velocity of topological defects. We show that the defects interact with the interface at a specific interaction range, set by the vorticity length scale of flows within the colony, and that the cells predominantly reorient parallel to the interface due to division-induced active stresses.

Instabilities and topological defects in active nematics

Abstract: We study a continuum model of an extensile active nematic to show that mesoscale turbulence develops in two stages: i) ordered regions undergo an intrinsic hydrodynamic instability generating walls, lines of strong bend deformations; ii) the walls relax by forming oppositely charged pairs of defects. Both creation and annihilation of defect pairs reinstate nematic regions which undergo further instabilities, leading to a dynamic steady state. We compare this with the development of active turbulence in a contractile active nematic.

Journal of Fluid Mechanics创刊50周年

Abstract: 流体力学杂志“Journal of Fluid Mechanics”由剑桥大学教授George Batchelor在1956年5月创办，在国际流体力学界享有很高的学术声望，被公认为是流体力学最著名的学术刊物之一，2005年的影响因子为2．061，雄居同类期刊之首．在它创刊50周年之际，2006年5月JFM出版了第554卷的纪念特刊，其中刊登了现任主编（美国西北大学S．H．Davis教授和英国剑桥大学T．J．Pedley教授）合写的述评：“Editorial：JFM at50”，以JFM为背景，从独特的视角对近50年来流体力学的发展进行了简明的回顾和展望，并归纳了一系列非常有启发性的有趣统计数字．2006年7月21日在剑桥大学应用数学和理论物理研究所（DAMTP）举行了创刊50周年的庆祝会．下午2点，JFM的新老编辑和来宾会聚一堂，Pedley教授致开幕词，其后是5个精彩的报告：The mysterious rattleback and its fluid counterpart（Keith Moffatt），Developments in shear instabilities（Patrick Huerre），Falling clouds（Elisabeth Guazzelli），Ecotectural fluid mechanics（Paul Linden），The success of JFM（Herbert Huppert），最后由Davis教授致闭幕词．

Active gel physics

Abstract: The mechanical behaviour of cells is largely controlled by a structure that is fundamentally out of thermodynamic equilibrium: a network of crosslinked filaments subjected to the action of energy-transducing molecular motors. The study of this kind of active system was absent from conventional physics and there was a need for both new theories and new experiments. The field that has emerged in recent years to fill this gap is underpinned by a theory that takes into account the transduction of chemical energy on the molecular scale. This formalism has advanced our understanding of living systems, but it has also had an impact on research in physics per se. Here, we describe this developing field, its relevance to biology, the novelty it conveys to other areas of physics and some of the challenges in store for the future of active gel physics. Equilibrium physics is ill-equipped to explain all of life’s subtleties, largely because living systems are out of equilibrium. Attempts to overcome this problem have given rise to a lively field of research—and some surprising biological findings.

Topological defects in epithelia govern cell death and extrusion.

Abstract: Epithelial tissues (epithelia) remove excess cells through extrusion, preventing the accumulation of unnecessary or pathological cells. The extrusion process can be triggered by apoptotic signalling, oncogenic transformation and overcrowding of cells. Despite the important linkage of cell extrusion to developmental, homeostatic and pathological processes such as cancer metastasis, its underlying mechanism and connections to the intrinsic mechanics of the epithelium are largely unexplored. We approach this problem by modelling the epithelium as an active nematic liquid crystal (that has a long range directional order), and comparing numerical simulations to strain rate and stress measurements within monolayers of MDCK (Madin Darby canine kidney) cells. Here we show that apoptotic cell extrusion is provoked by singularities in cell alignments in the form of comet-shaped topological defects. We find a universal correlation between extrusion sites and positions of nematic defects in the cell orientation field in different epithelium types. The results confirm the active nematic nature of epithelia, and demonstrate that defect-induced isotropic stresses are the primary precursors of mechanotransductive responses in cells, including YAP (Yes-associated protein) transcription factor activity, caspase-3-mediated cell death, and extrusions. Importantly, the defect-driven extrusion mechanism depends on intercellular junctions, because the weakening of cell-cell interactions in an α-catenin knockdown monolayer reduces the defect size and increases both the number of defects and extrusion rates, as is also predicted by our model. We further demonstrate the ability to control extrusion hotspots by geometrically inducing defects through microcontact printing of patterned monolayers. On the basis of these results, we propose a mechanism for apoptotic cell extrusion: spontaneously formed topological defects in epithelia govern cell fate. This will be important in predicting extrusion hotspots and dynamics in vivo, with potential applications to tissue regeneration and the suppression of metastasis. Moreover, we anticipate that the analogy between the epithelium and active nematic liquid crystals will trigger further investigations of the link between cellular processes and the material properties of epithelia.

Topology and dynamics of active nematic vesicles

Abstract: Engineering synthetic materials that mimic the remarkable complexity of living organisms is a fundamental challenge in science and technology. We studied the spatiotemporal patterns that emerge when an active nematic film of microtubules and molecular motors is encapsulated within a shape-changing lipid vesicle. Unlike in equilibrium systems, where defects are largely static structures, in active nematics defects move spontaneously and can be described as self-propelled particles. The combination of activity, topological constraints, and vesicle deformability produces a myriad of dynamical states. We highlight two dynamical modes: a tunable periodic state that oscillates between two defect configurations, and shape-changing vesicles with streaming filopodia-like protrusions. These results demonstrate how biomimetic materials can be obtained when topological constraints are used to control the non-equilibrium dynamics of active matter.