Том 85, № 1 (2024)

Molecular mechanisms of stress response are interesting from an evolutionary point of view, as they are often under natural selection. In this study, we reviewed the molecular mechanisms of reaction to temperature stresses on the example of a model organism Drosophila melanogaster, which had been studied in detail. We compared the reactions to heat and cold stresses and identified similar and specific molecular response mechanisms. The key processes common to responses to both types of stress were the increased expression of the HSP (heat shock proteins) and Turandot genes and the activation of serine-threonine protein kinase p38 MAPK. Heat stress also induced TORC2-mediated formation of stress granules, but cold stress led to the increase in the synthesis of calcium-binding protein DCA and cryoprotective protein FROST. Some similarity in reactions to heat and cold stress can be explained by the similar nature of the damage induced by these stresses and the multifunctionality of the proteins that provide stress responses. Probably, there was an evolutionary trade-off between tolerance to heat and cold stress in D. melanogaster: an increase in resistance to one stress has led to a decrease in resistance to another. Fruit flies at different life cycle stages demonstrated different sensitivity to temperature influences, and the mechanisms of response to them also partially differed. The comparison of the studies on the evolution of proteins involved in response to temperature stresses allowed us to conclude that these molecular mechanisms evolved rapidly in insects, and the conclusions obtained on D. melanogaster should be transferred to other animals, even within the Diptera, with great caution. Using the FlyBase database, we examined the localization of genes whose products were involved in response to temperature stresses in the Drosophila genome. 15 out of the 21 genes mentioned in the work were located on the third chromosome, 10 on its right arm. That allowed us to hypothesize an adaptive convergence of these genes in the genome of D. melanogaster. Perhaps this helped synchronize the regulation of their expression more precisely. Understanding the molecular mechanisms of insect response to temperature stresses can be of practical importance: to help predict the changes in the species’ habitat and their adaptation to rapidly changing climate conditions, as well as to contribute to the development of insecticides that can withstand insect pests and invasive species.

Cell (somatic) polyploidy is a general biological phenomenon characteristic of unicellular and multicellular animals and plants. In mammals, polyploid cells occur in all tissues; in some cases they are few in number, while in other cases they may be the most numerous cells in an organ. The mechanism of polyploidization is a usual, but incomplete, mitosis. The cause of incompletion of the mitosis is competition between proliferation and differentiation. At the genome level, the cause is associated with metabolic disorders of cyclin-dependent kinases, some other mitotic kinases (AURORA), transcription factors Ect2, E2F, some regulatory proteins (p53, laminin, septin), and components of the Hippo signalling pathway. The timing of polyploidization is restricted to early postnatal ontogenesis and, as experiments with heart transplants have shown, is part of the developmental programme. A typical way of genome multiplication is the change from binucleate to polyploid mononucleate cells from cycle to cycle. Polyploidization of cells is irreversible. It is a normal mechanism of organ growth and, for some cells, a way of differentiation. Using cardiac muscle and liver as examples, it has been shown that the composition and number of polyploid cells depend on the life conditions in the early postnatal period. After leaving the mitotic cycle, the cells continue to grow; postmitotic hypertrophy is one of the main ways of the growth of the cardiac muscle in ontogenesis and the only way of its regeneration. A certain growth reserve of the cardiac muscle in case of damage (heart attack, etc.) has been revealed, which is associated with its ploidy formed in childhood. In case of damage to mammalian liver, all hepatocytes enter the cycle and both cell division and polyploidization occur. Polyploidy in the course of ontogenesis up to the stage of aging fully complements the restoration of tissue and organ activity.