Plants have the ability to recognize beneficial and pathogenic microorganisms. They can promote or limit their colonization as it is crucial for their survival. Plant hormones regulate plant microbe interactions, coordinate cellular and metabolic responses in relation to colonization by microorganisms (Boivin et al., 2016). Activation of plant immunity require signaling and control. As soon as the plant detects pathogen attack, the information is communicated through molecular signaling network to activate immune response.  The signaling network is highly interconnected and the common network component mediate different signaling event to inhibit each other (Sato et al., 2010). The signaling network are modulated in order to help plant to mitigate infection. The synergism between CK and SA promote defense against biotrophs. CK may promote jasmonic acid (JA); however in a feedback loop JA suppresses CK responses. The cross talk between auxin and cytokinin may have an antagonistic effect on plant immunity (Naseem et al., 2015). Insect or pathogen attack is followed by enhanced level of cytokinins (CKs) at the infection site. Increased  accumulation of CK   at infection site may decrease energy supply for plant growth but can fuel the plant defense machinery, suggesting that that these molecule play a key role in reconfiguration of the primary and secondary metabolism associated with plant –induced defense (Giron et al., 2013).  

Cytokinin phytohormone stimulate cell division and are involved in embryonic cells, maintenance of meristematic cells, shoot formation and development of vasculature.  This (CK) phytohormone is not only essential for plant growth and development but also impacts plant immunity (Wang et al., 2017). CK works as a major factor in plant-microbe interaction during nodule organogenesis and pathogenesis. Plant-borne cytokinins systemically induce resistance against pathogen infection. This resistance is by endogenous CK and salicylic acid (SA) signaling (Choi et al., 2011).  Plant pathogens manipulate the endogenous CK and/or auxin content of their host plant (Jameson 2000).

The CK signaling pathway regulates reactive oxygen species (ROS)  and homeostasis in guard cells which leads to enhanced stomatal immunity and plant resistance to bacteria (Arnaud et al., 2017). Stomata play a critical role in plant immunity. Upon pathogen attack or pathogen-associated molecular patterns (PAMPs) plants close their stomata to prevent invasion of pathogen and colonize the host tissue (Melotto et al., 2006). In turn pathogen virulence factor such as the phytotoxin coronatine (COR) secreted by the bacterial pathogen Pseudomonas syringae pv tomato (Pst) strain DC3000 suppresses host stomatal defenses and further advance stomatal reopening (Melotto et al., 2006).

Plant hormone change host immunity. The concentration of CK regulates defense responses in a positive or a negative manner i.e. cytokinin level influence the outcome of plant-pathogen interactions.  Argueso et al. (2012) observed that high concentration of CK lead to increased defense responses to a virulent oomycete pathogen, through SA accumulation and activation of defense gene expression. Lower concentration of CK results in increased pathogen growth. Novak et al. (2013) suggested that plant can produce sufficiently high levels of cytokinins to trigger fast cell death without any interveining chlorosis- symptom for hypersensitive response. The chloroplastic hydrogen peroxide stimulates hypersensitive-like response, including inhibition of photosynthesis, elevated levels of stress hormones, oxidative membrane damage and stomatal closure. 

 The cross talk between CK and SA signaling network regulate plant defense responses against pathogens.  Plant pathogen can trigger symptoms that indicate hormonal disorders, formation of   galls, cankers of trees and premature senescence (so called green islands) in plants (Grant and Jones 2009). Pathogen can secrete CKs themselves or induce CK biosynthesis in plants or both leading to the suppression of plant immunity (Spallek et al., 2018). The accumulation of CK induces production and accumulation of phytoalexins in a SA-independent manner enhancing SA-dependent immunity (O’Brien and Benkova 2013). High CK levels, induced after the pathogen attack, activate CK signaling  pathway  which regulates pathogenesis related protein 1 (PR1), PR3, PR4 and PR5 expression hence promotes plant immunity (Naseem et al., 2012; O’Brien and Benkova 2013).

Cytokinins and auxins are known to act antagonistically, but a synergistic interaction between auxin and cytokinin also exists (Schaller et al., 2015). Jiang et al. (2013) reported CK accumulation after infection by blast fungus Magnaporthe oryzae .  Fungus elevates rice CK levels for its own benefit such as mobilizing nutrients towards the infection site. On the other hand rice plant, sense CK accumulation as an infection signal and induces defense responses by   acting synergistically with SA. Auxin inhibits CKs ranging from its biosynthesis to the suppression of its signaling (Naseem and Dandekar 2012). Cytokinin induced resistance is mediated by increased antimicrobial phytoalexin production (Grosskinsky et al., 2011). This demonstrates that auxin, abscisic acid, gibberellins and cytokinin cross communicate with the central ethylene-salicylic acid-jasmonic acid signal transduction pathway in immunity. The two phytoalexin such as scopoletin and capsidiol are often restricted to infected tissue (Grosskinsky et al., 2011).  Interestingly despite the absence of hypersensitive response, the increased level of CK induce bactericidal activities controlling bacterial growth. Plant needs to balance the two conflicting demands: efficiently abolish the pathogen infection and limit the negative impacts of immune responses on plant health (tissue integrity, photosynthetic capacity and primary metabolism) (Sato et al., 2010). High level of defense activation leads to reduced growth and reduced seed set. Impact of cytokinin has been observed on various aspects of plant immunity.

                                                         See Part IV for further information

                                                         Continue ……..


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