Cross Talk between Viruses and Insect Cells Cytoskeleton

Viruses are excellent manipulators of host cellular machinery, behavior, and life cycle, with the host cell cytoskeleton being a primordial viral target. Viruses infecting insects generally enter host cells through clathrin-mediated endocytosis or membrane fusion mechanisms followed by transport of the viral particles to the corresponding replication sites. After viral replication, the viral progeny egresses toward adjacent cells and reaches the different target tissues. Throughout all these steps, actin and tubulin re-arrangements are driven by viruses. The mechanisms used by viruses to manipulate the insect host cytoskeleton are well documented in the case of alphabaculoviruses infecting Lepidoptera hosts and plant viruses infecting Hemiptera vectors, but they are not well studied in case of other insect–virus systems such as arboviruses–mosquito vectors. Here, we summarize the available knowledge on how viruses manipulate the insect host cell cytoskeleton, and we emphasize the primordial role of cytoskeleton components in insect virus motility and the need to expand the study of this interaction.

Hydration–dehydration of cell cytoskeleton proteins and the problem of aging

The role of water in cell cytoskeleton proteins and the change in its volume under the influence of temperature are considered. The mechanism of cell pulsation is proposed, the leading factor of which is

Cancer cell cytoskeleton behavior on titanium oxides synthesized through ultrafast pulsed laser irradiation

Conventionally, single phases of TiO2 are used for targeted therapy and a drug carrier systems. In this research a harmonized approach in synthesizing multi-Ti oxide phases in a nanostructure and its ability to control cancer cell cytoskeleton behavior. This modulation of HeLa cancer cell cytoskeleton behaviour including shape of the cell, surface area of the cell, alignment of the cell is diligent by using the combination of TiO, Ti3O, Ti2O phases. Field emission scanning electron microscope investigation (FESEM) revealed that multi-Ti oxide nanostructure revealed a greater reduction of HeLa cell relative to fibroblast cell. This altered cell adhesion was followed by modulation of HeLa cell architecture with significant reduction in actin stress fibers. The intricate combination of multi-Ti oxide nanostructures renders a biomaterial that can precisely alter HeLa cell but not the fibroblast cell behaviour has the potential application of creating a multi-Ti oxide nanostructure for targeted cancer therapy, developing nano patterning devices. This unique interaction of HeLa cancer cell with multi-Ti oxide nanostructure has provided an insight of cell-cell signalling which is the fundamental mechanism in regulating their proliferative characteristics.

Cancer cell cytoskeleton behavior on titanium oxides synthesized through ultrafast pulsed laser irradiation

Conventionally, single phases of TiO2 are used for targeted therapy and a drug carrier systems. In this research a harmonized approach in synthesizing multi-Ti oxide phases in a nanostructure and its ability to control cancer cell cytoskeleton behavior. This modulation of HeLa cancer cell cytoskeleton behaviour including shape of the cell, surface area of the cell, alignment of the cell is diligent by using the combination of TiO, Ti3O, Ti2O phases. Field emission scanning electron microscope investigation (FESEM) revealed that multi-Ti oxide nanostructure revealed a greater reduction of HeLa cell relative to fibroblast cell. This altered cell adhesion was followed by modulation of HeLa cell architecture with significant reduction in actin stress fibers. The intricate combination of multi-Ti oxide nanostructures renders a biomaterial that can precisely alter HeLa cell but not the fibroblast cell behaviour has the potential application of creating a multi-Ti oxide nanostructure for targeted cancer therapy, developing nano patterning devices. This unique interaction of HeLa cancer cell with multi-Ti oxide nanostructure has provided an insight of cell-cell signalling which is the fundamental mechanism in regulating their proliferative characteristics.

Cell Cytoskeleton and Stiffness Are Mechanical Indicators of Organotropism in Breast Cancer

Tumor metastasis involves the dissemination of tumor cells from the primary lesion to other organs and the subsequent formation of secondary tumors, which leads to the majority of cancer-related deaths. Clinical findings show that cancer cell dissemination is not random but exhibits organ preference or organotropism. While intrinsic biochemical factors of cancer cells have been extensively studied in organotropism, much less is known about the role of cell cytoskeleton and mechanics. Herein, we demonstrate that cell cytoskeleton and mechanics are correlated with organotropism. The result of cell stiffness measurements shows that breast cancer cells with bone tropism are much stiffer with enhanced F-actin, while tumor cells with brain tropism are softer with lower F-actin than their parental cells. The difference in cellular stiffness matches the difference in the rigidity of their metastasized organs. Further, disrupting the cytoskeleton of breast cancer cells with bone tropism not only elevates the expressions of brain metastasis-related genes but also increases cell spreading and proliferation on soft substrates mimicking the stiffness of brain tissue. Stabilizing the cytoskeleton of cancer cells with brain tropism upregulates bone metastasis-related genes while reduces the mechanoadaptation ability on soft substrates. Taken together, these findings demonstrate that cell cytoskeleton and biophysical properties of breast cancer subpopulations correlate with their metastatic preference in terms of gene expression pattern and mechanoadaptation ability, implying the potential role of cell cytoskeleton in organotropism.

A novel in silico method for the molecular mimicry detection finds a formin with the potential to manipulate maize cell cytoskeleton

Molecular mimicry is one of the evolutionary strategies that parasites use to manipulate the host metabolism and perform an effective infection. This phenomenon has been observed in several animal and plant pathosystems. Despite the relevance of this mechanism in pathogenesis, little is known about it in fungus-plant interactions. For that reason, we performed an in silico method to select plausible mimicry candidates for the Ustilago maydis-maize interaction. Our methodology uses a tripartite sequence comparison between the parasite, the host and non-parasitic organisms’ genomes. Furthermore, we use RNA-seq information to identify gene co-expression, and we determine subcellular localization to detect potential cases of co-localization in the imitator-imitated pairs. With these approximations, we found a putative extracellular formin in U. maydis with the potential to rearrange the host cell cytoskeleton. In parallel, we detect at least two maize genes involved in the cytoskeleton rearrangement differentially expressed under U. maydis infection; thus, this find increases the expectation for the potential mimicry role of the fungal protein. The use of several sources of data led us to develop a strict and replicable in silico methodology to detect molecular mimicry in pathosystems with enough information available. Furthermore, this is the first time that a genome-wide search has been performed to detect molecular mimicry in a U. maydis-maize system. Additionally, to allow the reproducibility of this experiment and the use of this pipeline, we create a Web server called Molecular mimicry finder, available in https://bioquimio.udla.edu.ec/molecular-mimicry/