**2. Auxins: major roles in plants under salinity stress**

Many physiological and developmental processes, including the formation of lateral and adventitious roots, flowering, senescence, and morphogenesis, are regulated by auxins, primarily indole-3 acetic acid (IAA) [13]. Auxin is one of the most significant phytohormones involved in the regulation of lateral root growth, main root elongation, and halotropism, the special capacity of plants to avoid salty circumstances when they are under salt stress. Auxin-mediated lateral root formation and the cessation of their growth in response to excessive salt have been shown to be antagonistic [14]. The gradient, concentration, and spatiotemporal expression of receptor genes tightly govern auxin's regulatory mechanisms [15]. The intense regulation of this phytohormone at several levels, as well as its manufacture and signaling, led to a drop in endogenous auxin levels being identified under salt stress [16]. Three key auxin sources exist in plants, namely synthetic auxin, endogenous auxin and microbial auxin sources from the rhizosphere [17].

#### **Figure 1.**

*Scheme representing the major structure of auxin and brassinosteroids, and their connection with salt stress.*

### *Control of Plant Responses to Salt Stress: Significance of Auxin and Brassinosteroids DOI: http://dx.doi.org/10.5772/intechopen.111449*

Auxin signal transduction pathway has been broadly examined [18, 19] and TIR1 encodes a nuclear auxin receptor belonging to the F-box protein [20] that interacts with a group of AUX/IAA (Auxin/Indole-3-Acetic Acid) proteins. Through their interaction with the transcriptional regulators of ARF (auxin response factors), AUX/ IAA operates as negative regulators by impeding transcriptional auxin output [21]. ARFs, with their 23 members, can therefore activate or repress target genes and mediate the auxin responses, and they are destroyed when auxin binds to TIR1 [22].

Several kinds of efflux/influx carriers control the auxin transport in the plant root, resulting in the auxin gradient. The auxin-resistant 1/like aux1 (AUX/LAX) family of influx carriers mediates an active polar transport [23]. On the other hand, auxin efflux transporters include ABC transporter family [24], NRT1/PRT family of nitrate transporter 1/peptide transporter [25], and PIN-FORMED carriers [26, 27]. PINs constitute a family of 7 proteins that are found in the plasma membrane and are thought to be involved in the control of auxin transport [17]. Salt stress lowers auxin levels, which in turn drops the expression of auxin transporters [16], linking auxin distribution and biosynthesis [28]. PIN abundance is primarily responsible for the disruption in auxin transport. The authors in [29] have discovered that the PIN2 auxin efflux carrier is the most specific to salt stress since it is seen to actively redistribute auxin in the root tip when exposed to a salt gradient. Auxin redistribution and directional bending of the root away from high salt levels are mediated by PIN2 internalization, which is stimulated by salt-induced phospholipase-D at the side of the root facing the higher salt concentration. Under salt stress, the downregulation of PIN1, PIN3 and PIN7 is also an important part of the asymmetric distribution of auxin, which affects root bending from the salt [15]. Furthermore, primary root size is abridged under salt stress alongside with a decrease in lateral root density due to decreased levels of PIN1, PIN3 and PIN7 [16].

Auxin carriers' function can be regulated through post-translational changes, subcellular localization, and regulation of their expression in addition to the regulation of their expression. In order to allow auxin redistribution and for the directional bending of the root away from the higher salt concentration, PIN2 and AUX1 alter their subcellular location in endosomes [29, 30]. AUX1 and PIN2 are required for the establishment of gravity-inducing asymmetric auxin response. Auxin transport in the elongation zone requires AUX1, but its transport back to the root tip is mostly mediated by PIN2 [31]. According to the model of [32] that was predicted to occur during halotropism, auxin asymmetry is caused by an imbalance in the PIN2 and AUX1 pathways in the root tip, with PIN2 decreasing on the side of the root that is exposed to salt and changing auxin levels on the opposite side. This asymmetry of auxin was amplified by the AUX1 auxin transporter. The AUX1 auxin transporter increased this auxin asymmetry.

What is trusty to mention is that PIN polarity and intracellular auxin polar fluxes are both required for PIN phosphorylation [33]. For instance, during phototropic and gravitropic reactions mediates PIN3 phosphorylation to establish an auxin gradient during phototropic and gravitropic responses [34]. The balanced actions of PID kinase and protein phosphatases do in fact regulate the status of phosphorylation in PINs. RCN1 (ROOTS CURL IN NPA 1) encodes a regulatory subunit of protein phosphatase 2A (PP2A). It has been reported that the mutant rcn1 shows an elevation in gravitropic root bending curvature [33–35]. Auxin biosynthesis is carried out by different reactions of the indole-3-acetaldoxime pathway mediated by enzymes like tryptophan aminotransferase (TAA)/YUCCA (YUC) [36]. The processes of IAA production, conjugation, and degradation determine the amounts of IAA in

cells. Firstly, the YUCCA (YUC) family of enzymes, which are present throughout the root system, controls IAA production [37]. Auxin redistribution caused by the movement of auxin production from columella cells to the root epidermis during salt stress is partially connected with a reduction in the growth of primary and lateral roots [38]. Interestingly, YUC gene expression is calibrated in response to salt stress [39]. In fact, transcriptomic data show that YUC5 is up-regulated immediately after salt exposure [40] demonstrating that this gene plays a major role in auxin-mediated salt stress response.

Secondly, IAA levels are impacted by both conjugation and degradation processes, as observed through the positive correlation between free IAA levels and the levels of IAA conjugates and catabolites in roots and shoots. The degradation of IAA is the primary factor responsible for its rapid turnover and is mainly catalyzed by DAO1 and 2. A study has shown that DAO1/2 plays a crucial role in the root response to salt stress induced by lateral root density. Indole-3-butyric acid (IBA) contributes significantly to lateral root growth, root hair elongation, and adventitious root formation during root development. However, IBA can undergo oxidation and transform into IAA, which can negatively impact a plant's ability to tolerate salinity [41]. The irreversible conjugation of aspartic acid to IAA tags it for oxidation as well as for catabolism and IAA-asp conjugates are known to be involved in IAA detoxification [42].

It has been established that abiotic stress, particularly salt, has an impact on these processes. The GH3 (Gretchen Hagen) family of enzymes can catalyze the addition of some groups and generate diverse auxin conjugate genes (i.e: ILR/IAR (IAAamido hydrolase) and ILL (ILR1 likes)). Salt stress tolerance is mediated in part by auxin homeostasis, which is controlled by a collection of GH3 enzymes through a negative feedback regulation. WES1 (a kind of GH3) gene regulation is essential for salt stress tolerance [43]. Indeed, GH3 gene family is a desirable option for salt stress breeding since it is extensively expressed in roots and is increased when exposed to salt stress [39].
