Search

Cell fusion takes place in all domains of life and contributes greatly to the formation of complex multicellular structures. In particular, many fungi, such as the filamentous Neurospora crassa, rely on conspecific somatic cell fusion to drive the unicellular-to-multicellular transition and formation of the interconnected mycelial syncytium. This can, however, lead to the transmission of infectious elements and deleterious genotypes that have a negative impact on the organismal fitness. Accumulating evidence obtained from natural populations suggests that N. crassa has evolved various self/non-self or allorecognition systems to avoid fusion between genetically non-identical spores or hyphae at all costs. Here we present an overview of the recent advances made in the field of fungal allorecognition, describe its genetic basis, and comment on its evolutionary meaning. These data pinpoint the multilayered complexity of the cooperative social behaviors undertaken by a model eukaryotic microbe.

Cell fusion takes place in all domains of life and contributes greatly to the formation of complex multicellular structures. In particular, many fungi, such as the filamentous Neurospora crassa, rely on conspecific somatic cell fusion to drive the unicellular-to-multicellular transition and formation of the interconnected mycelial syncytium. This can, however, lead to the transmission of infectious elements and deleterious genotypes that have a negative impact on the organismal fitness. Accumulating evidence obtained from natural populations suggests that N. crassa has evolved various self/non-self or allorecognition systems to avoid fusion between genetically non-identical spores or hyphae at all costs. Here we present an overview of the recent advances made in the field of fungal allorecognition, describe its genetic basis, and comment on its evolutionary meaning. These data pinpoint the multilayered complexity of the cooperative social behaviors undertaken by a model eukaryotic microbe.

The metastatic process is arduous. Cancer cells must escape the confines of the primary tumor, make their way into and travel through the circulation, then survive and proliferate in unfavorable microenvironments. A key question is how cancer cells overcome these multiple barriers to orchestrate distant organ colonization. Accumulating evidence in human patients and animal models supports the hypothesis that clusters of tumor cells can complete the entire metastatic journey in a process referred to as collective metastasis. Here we highlight recent studies unraveling how multicellular coordination, via both physical and biochemical coupling of cells, induces cooperative properties advantageous for the completion of metastasis. We discuss conceptual challenges and unique mechanisms arising from collective dissemination that are distinct from single cell-based metastasis. Finally, we consider how the dissection of molecular transitions regulating collective metastasis could offer potential insight into cancer therapy. [ABSTRACT FROM AUTHOR]

The article presents the results of the research of CD3/CD28-induced production of interleukin-2 by blood lymphocytes in vitro as well as subpopulation composition of peripheral blood T-lymphocytes in patients with drug-sensitive and drug-resistant pulmonary tuberculosis. We detected the decrease in the total amount of CD3-positive cells and suppression of IL-2- secretion during CD3/CD28-induction of lymphocytes, which was most expressed in a disseminated form of drug-resistant TB. We also demonstrated the reduction in the percentage value of CD3+CD28+IL-2+ and CD3+CD28+IL-2- cells in patients with pulmonary TB against the background of the increase in the percentage value of CD3+CD28-IL-2-. Besides, it was also shown that the detected changes are unidirectional, don't depend on a clinical form of TB and are maximally manifested in patients with a drug resistant variant of the TB process.

Considering the data on the low level of self-organization (self-synchronization) of protein synthesis rhythm in aging, we studied the possible interference of the signaling factors of self-organization, gangliosides and catecholamines, as well as catecholamine reception. Experiments were carried out on primary cultures of rat hepatocytes on slides. Inhibited ganglioside synthesis did not prevent the organization of protein synthesis rhythm by the α-adrenomimetic agent phenylephrine. Upon the blockade of α-receptors by prazosin, the protein synthesis rhythm was observed after the exposure to gangliosides. α-Adrenolytic agents prazosin and benoxathian abolished the synchronizing effect of the β-adrenomimetic isoproterenol. A mixture of α-and β-adrenomimetic agents inhibited the protein synthesis rhythm-organizing effect of noradrenaline. Thus, the signaling molecules of self-organization of protein synthesis function independently via specific receptors. [ABSTRACT FROM AUTHOR]