Non-perturbative proton stability

Proton decay is a generic prediction of GUT models and is therefore an important channel to detect the existence of unification or to set limits on GUT models. Current bounds on the proton lifetime are around 10^33 years, which sets stringent limits on the GUT scale. These limits are obtained under `reasonable' assumptions about the size of the hadronic matrix elements. In this paper we present a non-perturbative calculation of the hadronic matrix elements within the chiral bag model of the proton. We argue that there is an exponential suppression of the matrix elements, due to non-perturbative QCD, that stifles proton decay by orders of magnitude -- potentially O(10^-10). This suppression is present for small quark masses and is due to the chiral symmetry breaking of QCD. Such a suppression has clear implications for GUT models and could resuscitate several scenarios

Quantum Feynman-Kac perturbations

We develop fully noncommutative Feynman-Kac formulae by employing quantum stochastic processes. To this end we establish some theory for perturbing quantum stochastic flows on von Neumann algebras by multiplier cocycles. Multiplier cocycles are constructed via quantum stochastic differential equations whose coefficients are driven by the flow. The resulting class of cocycles is characterised under alternative assumptions of separability or Markov regularity. Our results generalise those obtained using classical Brownian motion on the one hand, and results for unitarily implemented flows on the other.Comment: 27 pages. Minor corrections to version 2. To appear in the Journal of the London Mathematical Societ

Crumbling under Pressure

In order for an organism to maintain its form, it must be able to withstand physical perturbation, including the pull of gravity. A recent study in Nature from Porazinski and colleagues (2015) suggests that mechanisms promoting tissue tension are critical to resist the Earth’s downward pull

Intracellular signalling and intercellular coupling coordinate heterogeneous contractile events to facilitate tissue folding

Cellular forces generated in the apical domain of epithelial cells reshape tissues. Recent studies highlighted an important role for dynamic actomyosin contractions, called pulses, that change cell and tissue shape. Net cell shape change depends on whether cell shape is stabilized, or ratcheted, between pulses. Whether there are different classes of contractile pulses in wild-type embryos and how pulses are spatiotemporally coordinated is unknown. Here we develop a computational framework to identify and classify pulses and determine how pulses are coordinated during invagination of the Drosophila ventral furrow. We demonstrate biased transitions in pulse behaviour, where weak or unratcheted pulses transition to ratcheted pulses. The transcription factor Twist directs this transition, with cells in Twist-depleted embryos exhibiting abnormal reversed transitions in pulse behaviour. We demonstrate that ratcheted pulses have higher probability of having neighbouring contractions, and that ratcheting of pulses prevents competition between neighbouring contractions, allowing collective behaviour.National Institute of General Medical Sciences (U.S.) (Grant R00GM089826)National Institute of General Medical Sciences (U.S.) (Grant R01GM105984

Apical Sarcomere-like Actomyosin Contracts Nonmuscle Drosophila Epithelial Cells

Actomyosin networks generate contractile force that changes cell and tissue shape. In muscle cells, actin filaments and myosin II appear in a polarized structure called a sarcomere, in which myosin II is localized in the center. Nonmuscle cortical actomyosin networks are thought to contract when nonmuscle myosin II (myosin) is activated throughout a mixed-polarity actin network. Here, we identified a mutant version of the myosin-activating kinase, ROCK, that localizes diffusely, rather than centrally, in epithelial cell apices. Surprisingly, this mutant inhibits constriction, suggesting that centrally localized apical ROCK/myosin activity promotes contraction. We determined actin cytoskeletal polarity by developing a barbed end incorporation assay for Drosophila embryos, which revealed barbed end enrichment at junctions. Our results demonstrate that epithelial cells contract with a spatially organized apical actomyosin cortex, involving a polarized actin cytoskeleton and centrally positioned myosin, with cell-scale order that resembles a muscle sarcomere.National Institutes of Health (U.S.) (GM06806)American Heart Association (Grant-in-aid 14GRNT1888005)American Cancer Society (grant 125792-RSG-14-039-01-CS)National Institutes of Health (U.S.) (Pre-Doctoral Training Grant T32GM00728

Force transmission in epithelial tissues

In epithelial tissues, cells constantly generate and transmit forces between each other. Forces generated by the actomyosin cytoskeleton regulate tissue shape and structure and also provide signals that influence cells' decisions to divide, die, or differentiate. Forces are transmitted across epithelia because cells are mechanically linked through junctional complexes, and forces can propagate through the cell cytoplasm. Here, we review some of the molecular mechanisms responsible for force generation, with a specific focus on the actomyosin cortex and adherens junctions. We then discuss evidence for how these mechanisms promote cell shape changes and force transmission in tissues

A model for gelation with explicit solvent effects: Structure and dynamics

We study a two-component model for gelation consisting of $f$-functional monomers (the gel) and inert particles (the solvent). After equilibration as a simple liquid, the gel particles are gradually crosslinked to each other until the desired number of crosslinks has been attained. At a critical crosslink density the largest gel cluster percolates and an amorphous solid forms. This percolation process is different from ordinary lattice or continuum percolation of a single species in the sense that the critical exponents are new. As the crosslink density $p$ approaches its critical value $p_c$, the shear viscosity diverges: $\eta(p)\sim (p_c-p)^{-s}$ with $s$ a nonuniversal concentration-dependent exponent.Comment: 6 pages, 9 figure

Actomyosin Pulsing in Tissue Integrity Maintenance during Morphogenesis

The actomyosin cytoskeleton is responsible for many changes in cell and tissue shape. For a long time, the actomyosin cytoskeleton has been known to exhibit dynamic contractile behavior. Recently, discrete actomyosin assembly/disassembly cycles have also been observed in cells. These so-called actomyosin pulses have been observed in a variety of contexts, including cell polarization and division, and in epithelia, where they occur during tissue contraction, folding, and extension. In epithelia, evidence suggests that actomyosin pulsing, and more generally, actomyosin turnover, is required to maintain tissue integrity during contractile processes. This review explores possible functions for pulsing in the many instances during which pulsing has been observed, and also highlights proposed molecular mechanisms that drive pulsing