Relaxation and Noise-Driven Oscillations in a Model of Mitotic Spindle Dynamics.

During cell division, the mitotic spindle moves dynamically through the cell to position the chromosomes and determine the ultimate spatial position of the two daughter cells. These movements have been attributed to the action of cortical force generators which pull on the astral microtubules to position the spindle, as well as pushing events by these same microtubules against the cell cortex and plasma membrane. Attachment and detachment of cortical force generators working antagonistically against centring forces of microtubules have been modelled previously (Grill et al. in Phys Rev Lett 94:108104, 2005) via stochastic simulations and mean-field Fokker-Planck equations (describing random motion of force generators) to predict oscillations of a spindle pole in one spatial dimension. Using systematic asymptotic methods, we reduce the Fokker-Planck system to a set of ordinary differential equations (ODEs), consistent with a set proposed by Grill et al., which can provide accurate predictions of the conditions for the Fokker-Planck system to exhibit oscillations. In the limit of small restoring forces, we derive an algebraic prediction of the amplitude of spindle-pole oscillations and demonstrate the relaxation structure of nonlinear oscillations. We also show how noise-induced oscillations can arise in stochastic simulations for conditions in which the mean-field Fokker-Planck system predicts stability, but for which the period can be estimated directly by the ODE model and the amplitude by a related stochastic differential equation that incorporates random binding kinetics.

Confined migration: Microtubules control the cell rear.

Cell migration through complex 3D environments relies on the interplay between actin and microtubules. A new study shows that, when cells pass through narrow constrictions, CLASP-dependent microtubule stabilisation at the cell rear controls actomyosin contractility to enable nuclear translocation and preserve cell integrity.

Secretory organelles of pathogenic protozoa

Processos de secreção celular desempenham papel relevante na biologia e no ciclo de vida de protozoários patogênicos. A presente revisão analisa, sob uma perspectiva de biologia celular, o processo de secreção em (a) micronemas, roptrias e grânulos densos encontrados em membros do grupo Apicomplexa, onde essas estruturas participam da penetração do protozoário no interior da célula hospedeira, na sua sobrevivência intravacuolar e no posterior egresso da célula hospedeira, (b) a fenda de Maurer, encontrada em Plasmodium, uma estrutura envolvida na secreção de proteínas sintetizadas pelo protozoário intravacuolar e transportada, através de vesículas, para a superfície do eritrócito, (c) a secreção de macromoléculas na bolsa flagelar de tripanosomatídeos, e (d) a secreção de proteínas que fazem parte da parede cística de Giardia e Entamoeba e que se concentram nas vesículas de encistamento.

Behaviour of microtubules in cells infected with Toxoplasma gondii

Toxoplasma gondii proliferates within the parasitophorous vacuole of the host cell. Simultaneously with parasite division and vacuolar development, lipids traffic and change in the spatial distribution of organelles of the host cell cytoplasm occur. Using fluorescence microscopy, and antibodies recognizing tubulin, we showed that microtubules change their distribution during host cell infection by tachyzoites of T. gondii. In addition, transmission electron microscopy of thin sections and replicas of partially extracted cells showed that host cell microtubules concentrate around the parasitophorous vacuole. Such microtubules distribution was evident in early infection times and was more prominent after 24 h of infection, when parasitophorous vacuole was completely surrounded by microtubules. However, the meshwork microtubule filaments became slack or absent after 72 h of infection of host cell. Colchicine and taxol treatment altered the shape of the parasitophorous vacuole containing tachyzoites. These observations suggest a close association between microtubules and intravacuolar development of parasites.

Role of the microtubular system in platelet aggregation

1. Four structural systems are involved in the process of platelet activation that leads to aggregation: 1) the membrane system, i.e., the cytoplasmic membrane, the dense tubular structure and the open canalicular structure; 2) alpha and dense granules; 3) the peripheral microtubular coils; 4) the microfibrillar meshwork of actin-myosin bundles. 2. We added four compounds which modify cell ultrastructure to normal platelet-rich plasma to analyze the behavior of the structural systems of platelet activation: vinblastine (100 micrograms/ml) and cimetidine (100 micrograms/ml) that act on the membrane system, ticlopidine (200 micrograms/ml) and colchicine (100 micrograms/ml) that affect primarily the microtubular structure, cytochalasin B (30 micrograms/ml) and phorbol myristate acetate (100 ng/ml) that act upon the granular system, and cytochalasin D (30 micrograms/ml) and concanavalin A (50 micrograms/ml) that influence the microfibrillar structure. Platelet aggregation was stimulated by epinephrine or thrombin. 3. Cimetidine and ticlopidine prevented aggregation. However, neither substance affected the microtubular structure. Colchicine and cytochalasin B only partially impaired aggregation, because pieces of microtubules remained in the presence of these substances. The other substances did not present anti-aggregant activity and did not preserve the microtubules. 4. We infer that the disappearance of the microtubules is necessary to produce aggregation. When they remain intact no aggregation is produced, even though the other structural systems are activated.