Plants have self-protection system in addition to morphological adaptation. Defense response in plants are the result of interaction of many genes in a network. Hormone signaling pathways are targeted by pathogen to disturb and evade plant defense responses. The stress related phytohormone salicylic acid (SA), jasmonic acid (JA) and ethylene (ET) participate in defense responses to mitigate pathogen effect. Plant hormones like abscisic acid (ABA), gibberellic acid (GA), cytokinin (CK), auxins and brassinosteroid (BR) play a critical role in plant-microbe interactions. BR regulates plant growth and defense, there can also be other hormones involved as well such as GA, ET, JA and SA. These different hormone interact to ensure specificity in response.
Brassinosteroids were originally identified as a group of growth-promoting hormones (Grove et al., 1979). Plant interactions with biotrophs, hemibiotrophs and necrotrophic pathogens are modulated by BR. However, BR induce resistance to biotrophs but susceptibility to most hemibiotrophs and necrotrophs (Yu et al., 2018). Plant immune system is able to detect invading microbes and trigger a defensive response against them. At the surface of plant cells, proteins called pattern recognition receptors (PRRs) are able to recognize specific molecules of microbes and pathogens i.e. plant use PRRs to sense conserved microbe- or pathogen-associated molecular patterns (MAMPs/PAMPS). BR signaling pathway has crosstalk with different MAMP/PAMP-triggered immunity (MTI or PTI) pathway at multiple level such as receptor, cytoplasmic or transcriptional levels (Yu et al., 2018). The growth promoting hormones BR have emerged as crucial regulator of the growth-immunity trade-off (Lozano-Duran and Zipfel 2015). BR-activated transcription factor BRASSINAZOLE RESISTANT 1 (BZR1) regulates many defense genes that negatively regulate immune response (Lozano-Duran et al., 2013).
BR signals are perceived by the BR receptor BRASSINOSTEROID INSENSITIVE1 (BRI1) and its coreceptor BRI1-ASSOCIATED KINASE 1 (BAK1) (Yu et al., 2018). BAK1 is a coreceptor for the plant brassinosteroid receptor, the leucine-rich repeat receptor kinase (LRR-RK) BRI1 (Belkhadir et al., 2012). Flagellin, the main protein of the bacterial flagella, elicit defence responses. Flagellin-sensitive2 (FLS2) is involved in flagellin recognition (Gomez-Gomez and Boller 2000). Recognition of flagellin by LRR-RK FLS2 may function in induced immunity by activating defense responses during plant-bacteria interaction.
BAK1 as co-receptor of pattern recognition receptor for both BR signaling and PAMP signaling may modulate the trade-off between plant growth and immunity (Kong et al., 2012). Receptors exist as independent monomer in absence of any ligand. BAK1 promotes BR and flagellin signaling through ligand induced interaction with BRI1 and FLS2. BAK1 is involved in signaling of other PAMPs to induce innate immunity response and also with signaling of unknown endogenous signal that restrict cell death (Gendron and Wang 2007). BAK1 is not only associated with developmental regulation through the plant hormone receptor BRI1 but also has a functional role in PRR-dependent signaling which initiates innate immunity (Chinchilla et al., 2007). BRI1-BAK1and FLS2-BAK1 complexes coexist in cells indicating that BAK1 might mediate the interplay between BR and PAMP signaling (Kong et al., 2012). Furthermore Belkhadir et al. (2012) observed that the synergistic activities of BRs on MAMP responses require BAK1 and that plant steroid homeostasis is critical in establishment of plant immunity. BR signaling modulates plant immunity during plant growth by regulating immune signaling.
In contrast to the view that BR enhance plant innate immunity De Vleesschauwer et al. (2012) reported that Pythium graminicola exploits endogenous BRs as virulence factors and hijacks the host BR machinery to cause disease. P. graminicola coopts the plant BR machinery as a decoy strategy to tap into immune signaling circuitry and interfere with effectual SA- and GA-controlled defences. BR antagonizes SA-mediated root immunity against pathogen P. gaminicola (De Vleesschauwer et al., 2012). It is demonstrated that brassinosteroid-mediated disease resistance (BDR) takes part in plant defense responses independently from SA-mediated defense responses (Nakashita et al., 2003). Albrecht et al. (2012) result, suggested that BR-mediated growth directly antagonizes innate immune signaling. They also observed that activation of BRI1 pathway leads to inhibition of PTI signaling mediated by several PRRs. BR production may contribute to the ability of the pathogen to suppress plant immunity.
BRs and GA undergo crosstalk with plant defense signaling pathways to fine-tune the regulatory role between growth and immunity (De Bruyne et al., 2014; Lozano-Duran and Zipfel 2015). BR is implicated in plant responses to pathogen attack. Exogenously applied BR confers tolerance to plant from a broad range of pathogen infection. BR-induced systemic resistance appears to be independent of the systemic acquired resistance (SAR) activated by necrotizing pathogens or by SAR inducers such as SA. Hence the possible existence of a steroid hormone–mediated disease resistance in BR-treated plant (Yu et al., 2018).
Brassinolide (BL) is a brassinosteroid that regulates plant growth and induce disease resistance in plants. BL has the ability to induce disease resistance in rice plants. In tobacco BL enhances resistance to the viral, bacterial and fungal pathogens (Nakashita et al., 2003). Nakashita et al. (2003) observed BL induces disease resistance in both tobacco and rice, the resistance is systemically induced in tobacco with a mechanism different from known induced resistance. Kemmerling et al. (2007) studied that BAK1 which operates as a coreceptor of BRI1 in brassinolide-dependent plant development, regulates the containment of infection-induced cell death. BAK1-deficient plant develop necrosis upon infection.
Plant receptor kinases may perform dual function for many plant. In tomato, the BRI1 ortholog is required for responses to both BR and peptide hormone systemin which activates the systemic wound responses (Scheer et al., 2003). Such dual function along with several LRR-RLK genes in plant genome (over 230 in Arabidopsis) allows plant to respond to internal and external signals (Gendron and Wang 2007). Programme cell death may act as a barrier to biotrophic pathogens but defense strategies that result into cell death make plant more susceptible to necrotrophic pathogen and therefore must be controlled.
See Part VI for further information
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