*3.1.3. ABA and desiccation tolerance*

which belongs to the LEA group 2 proteins, overactivates salt-stress-inducible genes such as *RD29B*, which encode dehydration protective proteins, and subsequently confers salt tolerance

In addition, ABA has been implicated in histone H3 acetylation and methylation, thereby regulating stress-inducible gene expression at the epigenetic level. Chen *et al.* [62] showed that histone modifications by HISTONE DEACETYLASE 6 (HDA6) are involved in inhibition of seed germination, salt stress responses, and ABA- and salt-mediated gene expression in

Drought is lack of water in the soil. Drought stress in plants arises due to water deficit conditions and results in removal of water from the cell membranes, disrupting the lipid bilayer structure. In addition, protein denaturation and accumulation of cellular electrolytes results in disruption of cellular metabolism [63]. Therefore, drought causes osmotic stress, and osmotic stress causes dehydration and inhibition of water uptake in plants. ABA accumulates under osmotic stress conditions and plays an important role in the stress response and tolerance of plants. In addition to autoactivation of SnRK2s by inhibition of PP2Cs in the ABA signaling cascade, hyperosmotic stress activates SnRK2s [64]. SnRK2 kinases are a major component of the osmotic stress signaling pathway. The Arabidopsis triple mutant *snrk2.2, snrk2.3, snrk2.6* shows severe drought intolerance and ABA-insensitivity [42]. Also ABF2, ABF3, and ABF4 act as transcriptional activators in mediating ABRE-dependent ABA signal‐

ABA induces expression of many transcription factors as well as genes that encode enzymes in the synthesis of osmoprotectants [65]. Osmolytes are compatible solutes such as amino acids (proline), sugar alcohols (mannitol, pinitol), and other sugars that accumulate without disrupting the function of proteins. Osmolytes make an osmotic adjustment facilitating a

Dehydrins and LEA-like proteins act as cellular chaperones that protect cellular membranes and macromolecules in the cell [2]. During seed maturation seeds undergo dehydration stress. LEA proteins accumulate in the embryo as a result of osmotic stress and their functions include protection of enzymes, lipids, and mRNAs from dehydration. LEA proteins have been found to protect mitochondrial membranes from damage. LEA proteins are produced in an ABA-

Under moderate water stress conditions plant root growth has to be maintained in order to keep the plants alive. ABA accumulates under moderate water stress and mediates auxin transport in the root tip, which enhances the proton pumps in the plasma membrane. Proton secretions in the root tip play an important role in primary root growth and root hair devel‐

Based on the critical water level, drought tolerance is considered to be mechanisms that confer tolerance to moderate dehydration. Further dehydration requires desiccation tolerance

mechanisms in order to restore the ability of cells to rehydrate successfully [68].

ing, which confers drought tolerance in vegetative tissues [40].

favorable water potential gradient and promote stress tolerance [66].

dependent and ABA-independent manner under osmotic stress [47,58].

opment under moderate drought stress [67].

in Arabidopsis.

Arabidopsis.

*3.1.2. ABA and drought tolerance*

516 Abiotic and Biotic Stress in Plants - Recent Advances and Future Perspectives

Water loss results in a change in turgor pressure that affects the cell walls. Desiccation tolerance is defined as evolution of cell walls that can withstand extensive water loss without damaging its structure or polymer organization. Desiccation tolerance mechanisms aim to restructure the cells walls and maintain normal growth under water stress conditions [69].

Regulation of the stomatal pore is crucial in adapting plants to abiotic stress by reducing extensive water loss. Stomatal opening and closing occurs as a result of turgor pressure differences in the surrounding guard cells [47]. In response to water stress, ABA concentration is increased in the guard cell cytoplasm and apoplast, which results in a decrease in the turgor pressure due to activation of the K+ outward rectifying channel and inhibition of the K+ inward rectifying channel (KAT1 and 2). ABA also induces the anion channel SLAC1 resulting in release of anionic organic acids from the vacuole to the cytoplasm [70]. Reduced turgor pressure initiates closure of stomata as a mechanism of minimizing water loss from the plant. ABA levels rise in leaves immediately following water stress. CHLH/ABAR has been proposed as the chloroplast ABA receptor that links ABA signaling within the chloroplast with ABA signaling in the nucleus. Overexpression of CHLH promotes stomatal closure and thereby dessication tolerance [71].

SnRK2 OPEN STOMATA 1 (OST1) is a key SnRK2 protein kinase involved in regulation of the stomatal aperture by movement of guard cells during ABA signaling [72]. OST1 is activated by ABA, low humidity, and osmotic stress and is an important kinase found in guard cells preventing rapid water loss. Loss of function mutants of SnRK2 do not exhibit ABA-mediated stomatal closure activity and showed a wilty phenotype under dehydration stress conditions [72,73]. Also SnRK2.6/OST1 physically interacts with ABI1 and ABI2. ABI1 is required for ABAdependent activation of OST1 and both ABI and ABI2 are required for osmotic-stress-induced activation of OST1 [15]. Thus, SnRK2.6/OST1 acts as a positive regulator in ABA-induced stomatal closure. Moreover, Yoshida *et al.* [73] showed that OST1 also positively regulates stress-responsive genes such as *RD29B* and *RD22*.

Reactive Oxygen Species (ROS) have also been identified as secondary messengers in ABA signaling in guard cells. In Arabidopsis, two partially redundant guard cell expressed NADPH oxidase catalytic subunit genes, *AtRbohD* and *AtRbohF,* were found to be involved in ABA signaling in guard cells, ABA-induced stomatal closure and ROS production, ABA activation of Ca2+ permeable channels in the plasma membrane of guard cells, and increasing cytosolic Ca2+ levels in response to ABA. Thus, these two genes act as positive regulators of ABA signal transduction [74]. Sirichandra *et al.* [72] provided biochemical evidence that OST1 protein kinase physically interacts with AtRbohF NADPH oxidase and phosphorylates it.
