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Cancer is widely regarded as a critical health issue in modern society. Tumour cells are usually associated with abnormal proliferation that disrupts the normal behaviour of the body. All cells depend on the availability of oxygen and nutrients present in the extracellular environment, which can enhance or decrease their ability to proliferate. Therefore, to comprehend the influence of these factors, it is helpful to understand the proliferation process of both healthy and tumour cells. Computational models are powerful tools used to study biomedical problems, and several models have been presented in the literature. Different numerical methods have been proposed to solve these models. Among them, meshless methods can be highlighted, as they are used to solve complex problems with accurate results. However, in the case of cell proliferation, this is still an area that has not yet been fully explored. The aim of this work is to implement and study the influence of oxygen and glucose during the proliferation of healthy and tumour cells using a novel algorithm. This is an iterative discrete algorithm that employs a meshless numerical and uses a new phenomenological law to describe cell growth. In the end, the algorithm was capable of generating satisfactory results, in accordance with the literature. [ABSTRACT FROM AUTHOR]

The sorting nexins family of proteins (SNXs) plays pleiotropic functions in protein trafficking and intracellular signaling and has been associated with several disorders, namely Alzheimer’s disease and Down’s syndrome. Despite the growing association of SNXs with neurodegeneration, not much is known about their function in the nervous system. The aim of this work was to use the nematode Caenorhabditis elegans that encodes in its genome eight SNXs orthologs, to dissect the role of distinct SNXs, particularly in the nervous system. By screening the C. elegans SNXs deletion mutants for morphological, developmental and behavioral alterations, we show here that snx-3 gene mutation leads to an array of developmental defects, such as delayed hatching, decreased brood size and life span and reduced body length. Additionally, ∆snx-3 worms present increased susceptibility to osmotic, thermo and oxidative stress and distinct behavioral deficits, namely, a chemotaxis defect which is independent of the described snx-3 role in Wnt secretion. ∆snx-3 animals also display abnormal GABAergic neuronal architecture and wiring and altered AIY interneuron structure. Pan-neuronal expression of C. elegans snx-3 cDNA in the ∆snx-3 mutant is able to rescue its locomotion defects, as well as its chemotaxis toward isoamyl alcohol. Altogether, the present work provides the first in vivo evidence of the SNX-3 role in the nervous system. [ABSTRACT FROM AUTHOR]

During cytokinesis, a contractile ring consisting of unbranched filamentous actin (F-actin) and myosin II constricts at the cell equator. Unbranched F-actin is generated by formin, and without formin no cleavage furrow forms. In Caenorhabditis elegans , depletion of septin restores furrow ingression in formin mutants. How the cleavage furrow ingresses without a detectable unbranched F-actin ring is unknown. We report that, in this setting, anillin (ANI-1) forms a meshwork of circumferentially aligned linear structures decorated by non-muscle myosin II (NMY-2). Analysis of ANI-1 deletion mutants reveals that its disordered N-terminal half is required for linear structure formation and sufficient for furrow ingression. NMY-2 promotes the circumferential alignment of the linear ANI-1 structures and interacts with various lipids, suggesting that NMY-2 links the ANI-1 network with the plasma membrane. Collectively, our data reveal a compensatory mechanism, mediated by ANI-1 linear structures and membrane-bound NMY-2, that promotes furrowing when unbranched F-actin polymerization is compromised. [Display omitted] • An anillin-dependent compensatory mechanism drives furrowing if F-actin is low • The disordered anillin N terminus forms linear structures under the plasma membrane • Non-muscle myosin II represents in independent membrane anchor during cytokinesis • The anillin ring constricts to form a cleavage furrow when septins are also reduced During cytokinesis in animal cells, an actin-based ring constricts at the cell equator to form the cleavage furrow. Lebedev et al. discover a compensatory mechanism mediated by linear anillin structures and membrane-bound myosin II that drives cleavage furrow formation and ingression in case actin ring assembly fails. [ABSTRACT FROM AUTHOR]

Cytokinesis is the last stage of cell division, which partitions the mother cell into two daughter cells. It requires the assembly and constriction of a contractile ring that consists of a filamentous contractile network of actin and myosin. Network contractility depends on network architecture, level of connectivity and myosin motor activity, but how exactly is the contractile ring network organized or interconnected and how much it depends on motor activity remains unclear. Moreover, the contractile ring is not an isolated entity; rather, it is integrated into the surrounding cortex. Therefore, the mechanical properties of the cell cortex and cortical behaviors are expected to impact contractile ring functioning. Due to the complexity of the process, experimental approaches have been coupled to theoretical modeling in order to advance its global understanding. While earlier coarse-grained descriptions attempted to provide an integrated view of the process, recent models have mostly focused on understanding the behavior of an isolated contractile ring. Here we provide an overview of the organization and dynamics of the actomyosin network during cytokinesis and discuss existing theoretical models in light of cortical behaviors and experimental evidence from several systems. Our view on what is missing in current models and should be tested in the future is provided. [ABSTRACT FROM AUTHOR]