Physiology of Salt Stress in Plants. Группа авторов. Читать онлайн. Newlib. NEWLIB.NET

Автор: Группа авторов
Издательство: John Wiley & Sons Limited
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Жанр произведения: Биология
Год издания: 0
isbn: 9781119700494
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of Crop Plants

      Accumulation of salt ions in the plant rhizosphere causes dual stress to the plants, the osmotic imbalance between the soil and root cells, and cellular ionic imbalance due to passive or active intake of salt ions. The salinity‐induced osmotic stress suppresses the water uptake by the plants immediately, which then triggers various physiological and metabolic adjustments in the plants. Osmotic stress inhibits the expansion of the root and shoot cells within minutes due to reduced turgor pressure (Fricke et al. 2004; Munns et al. 2000) and the stress signal transduced rapidly at a speed of the sound through different signaling cascades from the root to the shoot tissue for the closure of stomata to minimize water loss, which seizes shoot metabolism (Christmann et al. 2013; Shabala et al. 2016). The mechanosensitive ion channels of the leaf guard cells sense the drop in xylem pressure and participate in stomatal closure, reducing the CO2 exchange and photosynthetic assimilation (Shabala et al. 2016). For osmotic adjustment, plants start the intake of the salt ions from the soil, which then enters different root and shoot cells creating the ionic stress to plants (Shabala and Lew 2002).

      The NaCl dominates the saline soil, and, therefore, the Na+ is the most critical ion, which is assumed to pose toxic effects on the plant cell physiology and metabolism. For their survival and optimal physiological activity, the ionic homeostasis is essential in the plants, and different ion channels and transporters in root or shoot tissues are involved in this process. The Na+ enters into the root cells through the glutamate receptor‐like (GLRs) channels, cyclic nucleotide‐gated (CNGCs) nonselective cation channels, high‐affinity K+ transporters (HKT2, HAK5), Shaker‐type K+ channels (AKT1), the low‐affinity cation transporter (LCT1), and aquaporins (PIP2;1) (Zhao et al. 2020). The entry of salt ions to the root cells and the osmotic stress spikes the Ca2+ in the root cells activating the salt overly sensitive (SOS) signaling pathway for the extrusion of the excess Na+ out of the cell (Hong et al. 2019; Shi et al. 2002). The function of active Na+ extrusion from root cells to the soil is performed by the plasma membrane Na+/H+ antiporter named salt overly sensitive 1 (SOS1) antiporter (Shi et al. 2002).

      2.4.1 Effect of Salt Stress on Chlorophyll Biosynthesis, Chloroplast Functioning, and Photophosphorylation

      In addition to photosynthesis, the chloroplast is the hub of several other metabolic activities: the biosynthesis of chlorophyll, carotenoid, ABA, vitamins, amino acids, and fatty acids and lipids (Zhao et al. 2020). Therefore, any environmental stress affects the metabolic pathways that operate in the chloroplast. Minutes after the salt stress, the stomata are closed, suppressing the exchange of the CO2 resulting in photosynthesis inhibition. In the light reaction of photosynthesis, the electron generated from the photo‐oxidation of water passes through the electron transport chain (ETC) on the thylakoid membrane to the electron acceptor proteins and molecules in the stroma. The transfer of electrons through the ETC generates a proton gradient across the thylakoid membrane, creating a proton motive force (PMF). This PMF drives the function of the chloroplast ATP synthase for the synthesis of ATP from the ADP, a process defined as the photophosphorylation (Sudhir and Murthy 2004). The plants use the ATP produced by the photophosphorylation in their metabolic pathways that operates in the chloroplast.

      2.4.1.1 Chlorophyll Biosynthesis in Salt Stress

      2.4.1.2 Salt Stress Affects Chloroplast Function

      Salt stress affects chloroplast more severely than another organelle, as the ROS increases rapidly due to chlorophyll triplet and oxygen molecules produced due to the photolysis of water, leading to its destruction. The salt stress leads to increased Na+ and Cl concentrations and decreased K+ concentration inside chloroplasts resulting in the swelling of thylakoid and unstacking of grana, thereby altering the photosynthetic structure (Santos 2004). The regulation of K+ and Cl across the thylakoid membrane is important in regulating the pH difference, which regulates the photoprotective nonphotochemical quenching mechanism and optimal photosynthesis (Finazzi et al. 2015). Any sort of disorder in this mechanism due to insufficient K+ during salt stress in the chloroplast may hamper its photoprotective mechanism. Accumulation of anions in the chloroplast affects both the acceptor and donor sides of photosystem II (PSII) by binding to a specific site on PSII (Jajoo et al. 1994, 2005). When the anions permeate the membrane during the salt stress, the influx of protons to balance the resultant charge causes structural reorganization in thylakoid membranes resulting in energy redistribution. All these salt stress components ultimately upset the ionic balance within chloroplasts, resulting in poor photosynthetic performance and reduced growth and yield. A shift in anion balance has shifted the solar energy distribution from PSII to PSI, affecting the function of the water‐splitting complex and electron transport to and from the plastocyanin (Singh‐Rawal et al. 2011). At the same time, soluble cations also cause alteration in the excitation energy transfer in the photosynthetic system at physiological temperatures by affecting several primary processes in thylakoids: initial energy distribution or “spillover” from PSII to PSI and rate constant of nonphotochemical quenching (Wong et al. 1980).

      During salt stress, the maximum quantum yield of PSII (Fv/Fm), photochemical quenching coefficient, and electron transport rate decreases, whereas nonphotochemical quenching increases (Yang et al. 2020), possibly due to unstacking of the grana. The reduced photochemistry and carbon fixation lead to an increase in ROS production which are potent in damaging chloroplast and its membrane (Hernández et al. 1995). To cope with this situation, the level of enzymatic (catalase, ascorbate peroxidase, and glutathione reductase) and nonenzymatic (ascorbate, total carotenoids, phenolics, and flavonoids) antioxidants increases (Taïbi et al. 2016). The ROS production, especially H2O2, inhibits the synthesis of