An in-depth comparative analysis of the evolutionary features of non-specific immune mechanism formation in mon o cotyledonous ( Triticum aestivum L.) and dicotyledonous ( Helianthus annuus L.) plants has been conducted. The main focus is on the differential role of key protein families – ABC transporters, lipid transfer proteins (LTPs), and wall-associated k i nase receptors (WAKs) – in modulating immune signaling cascades in response to various pathogenic and stress factors. The study demonstrates that winter wheat effectively implements systemic acquired resistance (SAR) mechanisms, particularly through the functioning of ABCG transporters (e.g., Lr34), ensuring long-term, quantitative resistance to a wide range of microbial pathogens. In contrast, sunflower predominantly exhibits a localized immune response (LAR), where ROS signa l ing, activated via WAK receptors, plays a key role, ensuring rapid response to necrotrophic pathogens and abiotic factors. The analysis indicates significant functional divergence of orthologous proteins: in wheat, WAK receptors and LTPs are primarily involved in strengthening physical barriers, whereas in sunflower, WAKs function as primary damage sensors (DAMPs) and activators of local stress pathways, and LTPs participate in signaling processes and membrane stabilization. Different immune strategies correlate with physiological-anatomical features and evolutionary adaptation to dominant p a thogen types. The obtained results underscore the importance of integrating knowledge about the molecular mechanisms of non-specific immunity into breeding programs and biotechnological approaches to create cultivars with enhanced and dur a ble resistance. Unresolved questions, particularly regarding the precise activation mechanisms of WAK receptors, and pro s pects for further research are discussed.

The review analyzes current data on the molecular mechanisms employed by bacteria to suppress and evade plant defense responses. It presents the strategies used by various pathogenic bacteria to overcome protective barriers associated with the cell wall and cytoplasmic components, including the cytoskeleton, which play a crucial role in plant immune responses to pathogens. Particular attention is given to bacterial effector proteins translocated into plant cells via the Type III Secretion System (T3SS), aimed at suppressing plant innate immunity and interfering with additional defense-related cellular processes such as proteasome-mediated protein degradation, phytohormone signaling, c y toskeleton organization, vesicular trafficking, and gene expression. Promising chemical compounds and innovative strategies for the control of bacterial plant diseases are also discussed.

The review examines the main stages of cytokinin biosynthesis and metabolism with an emphasis on the important role of cytokinin oxidase/dehydrogenase (CKO

Sunflower broomrape ( Orobanche cumana Wallr., 1825) is a significant and challenging parasite in sunflower crops gl o bally, infesting approximately 16 million hectares. Annual global crop losses due to broomrape infestation reach about 2.3 billion EUR. Therefore, our work addresses the critical scientific task of determining the spread, harmfulness, and racial composition of broomrape, developing protective measures for sunflowers against this parasite,and assessing the resistance of sunflower hybrids to broomrape. A pot experiment was conducted to identify the racial composition of the parasite and the resistance of various sunflower hybrids. Sunflower hybrids were evaluated for resistance to broomrape in soil culture using a modified method and the roll method of seed germination. Broomrape is actively spreading from the northern steppe of Ukraine to the country's central, northern, and western regions. The sunflower hybrids ES Nirvana, ES Romantic, ES Genesis, ES Bella, ES Andromeda, Janis, ES Niagara, and ES Artik, which are tolerant to race G, showed some parasitic effects from broomrape, though the degree of damage was not severe. On average, each sunflower plant had 2 to 3 nodules of the parasite. No sunflower hybrids exhibiting complete immunity to broomrape were discovered. Since sunflower hybrids ES Nirvana, ES Romantic, ES Genesis, ES Bella, ES Andromeda, ES Janis, ES Niagara, and ES Artik, resistant to race G, were affected, broomrape races A-F (race 6) significantly infest sunflower crops. Sunflower hybrids resistant to broomrape race E should not be cultivated, as this may lead to further spread of the parasite and a reduction in yield. Due to the minimal damage to the su n flower hybrids resistant to race G, race H (race 8) has recently begun to emerge in sunflower crops. Research to identify these more aggressive (H and I) races of the parasite is hindered by the lack of differentiating lines of sunflower resistance and hyb r ids for identification. Unfortunately, no hybrids resistant to race H (race 8) exist. The best sunflower hybrids show resistance to race G (race 7). The differentiation of sunflower hybrids grown for resistance to this parasite was completed. It has been noted that the broomrape population displays a considerable level of virulence that can overcome the immunity present in the most resilient foreign-bred hybrids resistant to races E, F, and G of the parasite. The widespread accumulation of parasite races E, F, G, and H in sunflower crops is connected to the disruption of crop rotations and the excessive cultivation of hybrids of this crop, primarily resistant to races 5 (E) and 6 (F) of the parasite. The research findings can be applied in the region's farms for effective prote c tion against broomrape and in breeding programs aimed at creating sunflower hybrids resistant to new parasite races, as well as corn hybrids that enhance seed germination of this pathogen in the soil and promote their death through root secretions.

Проведено вивчення процесу зараження Оrobanche сumana різних гібридів соняшнику з неоднаковою стійкістю до паразиту для оцінки клітинних механізмів резистентності. Отримані результати свідчать про те, що усі гібриди соняшнику уражувалися патогеном. Проте ступінь зараження вовчком соняшнику була різною і залежала від неоднакової резистентності гібридів. Гібридів соняшнику, що мали повний імунітет до Orobanche cumana, не було виявлено. При зараженні вовчком реакція резистентності гібридів соняшнику не відбувалася на ранніх стадіях життєвого циклу паразита: перед прикріпленням, після проростання та прикріплення до коренів (до утворення гаусторія) і після формування гаусторія. В обговоренні проаналізовані клітинні механізми виникнення резистентності соняшнику до паразиту. Охарактеризовані молекулярно-генетичні аспекти вродженого імунітету рослин. Узагальнені молекулярні основи резистентності рослин до патогенів. Окреслені нові ефективні підходи контролю на соняшнику паразита Orobanche cumana. З’ясування певних молекулярно-генетичних механізмів стійкості різних гібридів до патогена відкриває новий перспективний напрямок у зменшенні інфікування гібридів паразитом через індукцію системної набутої резистентності (SAR) препаратами, що викликають утворення активних форм кисню і запускають захисні реакції рослин через програмовану смерть клітин у місцях зараження та обумовлюють некроз патогена. У цьому контексті наведені напрямки пошуку нових перспективних хімічних речовин, які можна буде використовувати для розроблення біологічних гербіцидів та фунгіцидів, що є індукторами системної стійкості, для контроля патогена. Розглянуті перспективні сполуки, які індукують роботу сигнальних систем АФК і запускають праймінг захисних реакцій та викликають системну стійкість проти патогенів для лікування вірусних, бактеріальних і фітоплазмових хвороб і контроля паразитичних рослин, які важко контролювати традиційними хімічними методами.

Biological stress and aging are traditionally understood primarily through stressor-specific molecular mechanisms, including osmoregulation, stress-signaling pathways, proteostasis impairment, mitochondrial dysfunction, membrane remodeling, and cellular senescence. Despite substantial differences in their initiating mechanisms, diverse stressors and age-related changes are often accompanied by a common functional consequence: a reduced capacity of the cell to reversibly reorganize its intracellular environment and restore a functionally competent state after stressor removal. Here, we propose a unified biophysical theory of aging and stress based on phase plasticity, which considers the capacity of cellular matter to undergo controlled and reversible physical reorganization as a potential integrative level linking molecular mechanisms with functional recovery. The central concept of the model is phase plasticity, defined as the capacity of the cytoplasm, membranes, biomolecular condensates, and intracellular compartments to transition between functionally distinct physical states while retaining the capacity for reversible restoration. On this basis, Phase Rigidity Syndrome (PRS) is introduced as a hypothetical integrative state that may emerge from the progressive and cumulative loss of phase plasticity. We propose that phase rigidity is associated with reduced molecular mobility, altered biomolecular condensate dynamics, impaired membrane fluidity, diminished proteostatic capacity, and delayed or incomplete recovery following stress. Under prolonged or repeated stress, these changes may mutually reinforce one another, promoting a transition from adaptive phase reorganization toward persistent phase rigidity and, under extreme conditions, phase collapse. The theoretical framework integrates the concepts of phase homeostasis, phase buffer, phase resilience, phase recovery, phase memory, phase threshold, and phase-transition window, and introduces a conceptual Phase Resilience Index (PRI) for characterizing the capacity of cells to maintain and restore phase organization. Importantly, PRS is not proposed as an established biological or clinical syndrome, nor is phase plasticity presented as a validated universal variable. Rather, the proposed framework represents a research hypothesis that requires experimental testing. The proposed theory does not replace existing molecular models of cellular stress and aging but introduces an additional biophysical level of integration, at which distinct primary perturbations may partially converge through changes in the capacity of cellular matter to undergo reversible physical reorganization. The scientific value of the framework will ultimately depend on whether measures of phase plasticity provide additional predictive information on cellular resilience and recovery beyond established molecular markers of stress and aging.