Facilitation, competition, and vegetation patchiness: from scale free distribution to patterns

A new technique for the modeling of perennial vegetation patchiness in the arid/semiarid climatic zone is suggested. Incorporating the stochasticity that affects life history of seedlings and the deterministic dynamics of soil moisture and biomass, this model is flexible enough to yield qualitatively different forms of spatial organization. In the facilitation-dominated regime, scale free distribution of patch sizes is observed, in correspondence with recent field studies. In the competition controlled case, on the other hand, power-law statistics is valid up to a cutoff, and an intrinsic length scale appears.     

Catalyst-induced growth with limited catalyst lifespan and competition

Spatially extended catalyst-induced growth processes are studied. This type of processes exists in all domains of biology, ranging from ecology (nutrients and growth), through immunology (antigens and lymphocytes) to molecular biology (signaling molecules initiating signaling cascades). The extinction-proliferation transition is considered for a system containing discrete catalysts (A) that induces the proliferation of a discrete reactant (B). The realization of this model on an infinite capacity d-dimensional discrete lattice for immortal catalysts has been previously considered (the AB model). It was shown that the adaptation of the reactants to the diffusive noise induced by stochastic fluctuations of catalyst density yields proliferation even if the average environmental conditions lead to extinction. This model is extended here to include more realistic situations, like finite lifespan of the catalysts and finite carrying capacity of the reactants. By using a combination of Monte Carlo simulation, percolation-theory-based estimations and an analytic perturbative analysis, the asymptotic behavior of these systems is studied. In both cases studied, it turns out that the overall survival of the reactant population at the long run is based on the size and shape of a typical single colony, related to the localized proliferation around spatio-temporal catalyst density fluctuations. If the density of these colonies (based on the lifetime of the spatial fluctuation and the carrying capacity of the medium) is large enough, i.e. above the percolation threshold, the reactant population survives even in (on average) hostile environment. This model provides a new insight on the population dynamics in chemical, biological and ecological systems.     

Stabilization of metapopulation cycles: toward a classification scheme

The stability of population oscillations in ecological systems is considered. Experiments suggest that in many cases the single patch dynamics of predator-prey or host-parasite systems is extinction prone, and stability is achieved only when the spatial structure of the population is expressed via desynchronization between patches. A few mechanisms have been suggested so far to explain the inability of dispersal to synchronize the system. Here we compare a recently discovered mechanism, based on the dependence of the angular velocity on the oscillation amplitude, with other, already known conditions for desynchronization. Using a toy model composed of diffusively coupled oscillators we suggest a classification scheme for stability mechanisms, a scheme that allows for either a priori (based on the system parameters) or a posteriori (based on local measurements) identification of the dominant process that yields desynchronization.     

Neuron-specific ablation of the Krabbe disease gene galactosylceramidase in mice results in neurodegeneration

Krabbe disease is caused by a deficiency of the lysosomal galactosylceramidase (GALC) enzyme, which results in the accumulation of galactosylceramide (GalCer) and psychosine. In Krabbe disease, the brunt of demyelination and neurodegeneration is believed to result from the dysfunction of myelinating glia. Recent studies have shown that neuronal axons are both structurally and functionally compromised in Krabbe disease, even before demyelination, suggesting a possible neuron-autonomous role of GALC. Using a novel neuron-specific Galc knockout (CKO) model, we show that neuronal Galc deletion is sufficient to cause growth and motor coordination defects and inflammatory gliosis in mice. Furthermore, psychosine accumulates significantly in the nervous system of neuron-specific Galc-CKO. Confocal and electron microscopic analyses show profound neuro-axonal degeneration with a mild effect on myelin structure. Thus, we prove for the first time that neuronal GALC is essential to maintain and protect neuronal function independently of myelin and may directly contribute to the pathogenesis of Krabbe disease.

Krabbe disease is a demyelinating neurodegenerative disorder caused by a deficiency of the enzyme lysosomal galactosylceramidase (GALC), which results in the accumulation of galactosylceramide and psychosine. This study uses a novel neuron-specific knockout model in the first in vivo attempt to investigate the role of neuronal GALC in neuronal function and the etiology of Krabbe disease.     

Identification of Two Distinct Populations of Protein Kinase C in Rat Brain Membranes

The regulatory enzyme protein kinase C (PKC) is proposed to be activated on its translocation from the cytosol to the membrane. However, a portion of the native activity is always associated with the membrane fraction. Using a noninvasive procedure to extract this endogenous activity from rat brain membranes, it has been possible to characterize the activity in a partially purified reconstituted system bearing resemblance to the in vivo system. Two subpopulations of membrane-associated PKC were identified and characterized at the level of activation, inhibition, and isozyme immunologic characteristics and chromatographic properties. One peak had properties similar to those of cytosolic PKC, whereas the second population, extracted as protein-lipid complexes, had considerable constitutive activity that could be stimulated further on addition of PKC activators. This latter activity was relatively resistant to staurosporine inhibition and phorbol ester treatment, but it phosphorylated the exogenous PKC substrates, histone 1 and the epidermal growth factor receptor peptide KTRLRR. The constitutive activity was totally dependent on its endogenous associated lipids coextracted by the solubilization procedure. The ratio between these two populations was ontogenetically regulated and modulated by phorbol ester treatment, suggesting that different PKC populations may serve unique functions in the rat brain regulated by the lipid environment. Analyses of the phospholipids extracted in these protein-lipid complexes showed differences in the major classes correlating to age. However, apart from a markedly lower cholesterol content in these complexes, no direct relationship between a specific lipid composition and the amount of constitutive PKC activity was evident.     

Active mutants of the human p38alpha mitogen-activated protein kinase

Mitogen-activated protein (MAP) kinases compose a family of serine/threonine kinases that function in many signal transduction pathways and affect various cellular phenotypes. Despite the abundance of available data, the exact role of each MAP kinase is not completely defined, in part because of the inability to activate MAP kinase molecules individually and specifically. Based on activating mutations found in the yeast MAP kinase p38/Hog1 (Bell, M., Capone, R., Pashtan, I., Levitzki, A., and Engelberg, D. (2001) J. Biol. Chem. 276, 25351-25358), we designed and constructed single and multiple mutants of human MAP kinase p38alpha. Single (p38D176A, p38F327L, and p38F327S) and subsequent double (p38D176A/F327L and p38D176A/F327S) mutants acquired high intrinsic activity independent of any upstream regulation and reached levels of 10 and 25%, respectively, in reference to the dually phosphorylated wild type p38alpha. The active p38 mutants have retained high specificity toward p38 substrates and were inhibited by the specific p38 inhibitors SB-203580 and PD-169316. We also show that similar mutations can render p38gamma active as well. Based on the available structures of p38 and ERK2, we have analyzed the p38 mutants and identified a hydrophobic core stabilized by three aromatic residues, Tyr-69, Phe-327, and Trp-337, in the vicinity of the L16 loop region. Upon activation, a segment of the L16 loop, including Phe-327, becomes disordered. Structural analysis suggests that the active p38 mutants emulate the conformational changes imposed naturally by dual phosphorylation, namely, destabilization of the hydrophobic core. Essentially, the hydrophobic core is an inherent stabilizer that maintains low basal activity level in unphosphorylated p38.     

Nodal stability determines signaling range

Secreted TGFbeta proteins of the Nodal family pattern the vertebrate body axes and induce mesoderm and endoderm . Nodal proteins can act as morphogens , but the mechanisms regulating their activity and signaling range are poorly understood. In particular, it has been unclear how inefficient processing or rapid turnover of the Nodal protein influences autocrine and paracrine signaling properties . Here, we evaluate the role of Nodal processing and stability in tissue culture and zebrafish embryos. Removal of the pro domain potentiates autocrine signaling but reduces Nodal stability and signaling range. Insertion of an N-glycosylation site present in several related TGFbeta proteins increases the stability of mature Nodal. The stabilized form of Nodal acts at a longer range than the wild-type form. These results suggest that increased proteolytic maturation of Nodal potentiates autocrine signaling, whereas increased Nodal stability extends paracrine signaling.     

A model of herd grazing as a travelling wave,chemotaxis and stability

Possible constitutive models are examined for the formation of a herd, under the assumption that a herd forms a travelling wave while grazing. Under quite general conditions, it is found that the only possibility for a travelling wave is a balance between food seeking and natural dispersion, such as in chemotaxis. The stability of the travelling wave previously conjectured, is shown both for one- and two-dimensional perturbations.