Platelets play a key role in formation of hemostatic clots and obstructive thrombi as well as in other biological processes. In response to physiological stimulants, including thrombin, platelets change their morphology, express adhesive molecules, undergo aggregation, and secrete bioactive substances, but their subsequent fate is largely unknown. Here we examine late-stage structural, metabolic, and functional consequences of thrombin-induced platelet activation. Using a combination of confocal microscopy, scanning and transmission electron microscopy, flow cytometry, biochemical and biomechanical measurements, we show that thrombin-induced activation is followed by time-dependent platelet dysfunction and disintegration. After ~30 minutes of incubation with thrombin, unlike with collagen or ADP, human platelets underwent disintegration into cellular fragments containing organelles, such as mitochondria, glycogen granules, and vacuoles. Platelet fragmentation was preceded by Ca2+ influx, integrin αIIbβ3 activation and phosphatidylserine exposure (activation phase), followed by mitochondrial depolarization, generation of reactive oxygen species, metabolic ATP depletion and impairment of platelet contractility along with dramatic cytoskeletal rearrangements, concomitant with platelet disintegration (death phase). Coincidentally with the platelet fragmentation, thrombin caused calpain activation but not activation of caspases 3/7. Our findings indicate that the late functional and structural damage of thrombin-activated platelets comprise a calpain-dependent platelet death pathway that shares some similarities with the programmed death of nucleated cells, but is unique for this type of cell, therefore representing a special form of cellular destruction. Fragmentation of activated platelets suggests an underappreciated pathway for enhanced elimination of platelets from the circulation in (pro)thrombotic conditions once they have performed their functions.

Using an original methodological and technical approach, we studied the real-time dynamics of radial water transfer in roots and transpiration rate in intact maize plants in response to water stress. It was shown that the response of maize plants to water stress, induced by 10% PEG 6000, was accompanied by changes in the intensity and redistribution of water transfer along different pathways of radial water transport in the roots. It was shown that during the first minutes of water stress impact, the intensity of transcellular and symplastic water transport in the roots decreased with a parallel short-term increase in the transpiration rate in leaves and, presumably, in apoplastic transport in roots. Further, after a decrease in transpiration rate, the intensity of transcellular and symplastic water transport was restored to approximately the initial values and was accompanied by parallel upregulation of some PIP aquaporin genes in roots and leaves, changes in aquaporin localization in root tissues, and changes in xylem sap pH. Under water stress conditions, cell-to-cell water transport in roots becomes dominant, and aquaporins contribute to the simultaneous regulation of water transport in roots and shoots under water stress.

In the present study, we identified exopolysaccharides of the harmful phytopathogenic bacterium Pectobacterium atrosepticum SCRI1043 and characterized the molecular structure of these polymers. The synthesis of the target polysaccharides was shown to be induced under starvation conditions. Moreover, intensive accumulation of exopolysaccharides occurred during the colonization by bacteria of the xylem vessels of infected plants, where microorganisms formed specific 3D “multicellular” structures—bacterial emboli. Thus, the identified polymers are likely to be involved in the adaptation and virulence of bacteria of Pectobacterium genus.

Lichens often grow in microhabitats where they experience severe abiotic stresses. Some species respond to high UV radiation by synthesizing dark brown melanic pigments in the upper cortex. However, unlike the melanized structures of non-lichenized fungi, the morphology of the melanic layer in lichens remains unstudied. Here, we analyzed the morphology, ultrastructure, and elemental composition of the melanized layer in UV-exposed thalli of the lichen Lobaria pulmonaria (L.) Hoffm. Using light microscopy, we detected a pigmented layer sensitive to staining with 3,4-L-dihydroxyphenylalanine, a precursor of eumelanin, in the upper cortex of melanized thalli. Analysis of cross-sections of melanized thalli using scanning electron microscopy revealed that melanin-like granules are deposited into the hyphal lumens. Melanized thalli also possessed thicker hyphal cell walls compared to pale thalli. Energy-dispersive X-ray spectroscopy analysis of the elemental composition of the hyphal walls and extracted melanin indicated that the type of melanin synthesized by L. pulmonaria is eumelanin. Transmission electron microscopy was used to show that during melanization melanosome-like dark vesicles are transported to the cell surface and secreted into the cell walls of the fungal hyphae. Results from this study provide new insights into the effects of melanin synthesis on the microstructure of lichen thalli.