PLANT NEED ENERGY TO RESIST PATHOGENS

Plant when encounters pathogen induces many defense mechanism that involve redistribution of primary and secondary metabolites. Plant defense response to deal with the pathogen infection, is associated with increased demand for energy (Bolton 2009). The accumulation of free amino acid in pathogen-infected roots may reflect an increase demand for carbon. Tri carboxylic acid (TCA) in mitochondria generates energy. TCA oxidizes acetyl coenzyme A (acetyl-CoA) derived from carbohydrate, fatty acid, amino acid and ketones producing nicotinamide adenine dinucleotide hydrogen (NADH) and dihydro flavin adenine dinucleotide (FADH2). Besides this TCA provides intermediates that are utilized in synthesis of glucose, lipids and amino acid.

Plants require more energy to resist plant pathogen. Thus a shift from housekeeping to defense metabolism is in response to regulatory and signaling circuit. Energy is required for plant defense response due to expression of numerous gene from different defense pathway (Scheideler et al., 2002; Rojas et al., 2014). Some biotrophic bacteria colonize the apoplast and feed on apoplastic fluid, whereas, some biotrophic fungi establish via haustoria inside the plant cell that allow them to draw nutrient from cell. The hemibiotrophs first act as biotroph and later these hemibiotroph destroy the plant cell and feed on them as necrotrophic pathogen (Glazebrook 2005).

Recognition of pathogen is related with reprogramming of the plant cell metabolism. It is not clear that the accumulation of amino acids in the infected root results from the ability of the pathogen to reprogram the host metabolism or a host requirement to generate TCA intermediate for free amino acids which has a role in plant defense (Buhtz et al., 2015). The citrate and fumarate are two components of TCA cycle which can induce priming in Arabidopsis plant against the bacterial pathogen Pseudomonas syringae pv. tomato (Pst) DC3000 (Balmer et al., 2018). The citrate or fumarate has no antimicrobial effect, hence the resistance observed in plant is due to the induction of plant defense system. At an early stage of bacterial infection, citrate induced salicylic acid (SA) and at later stage accumulated camalexin by induction of jasmonic acid (JA) (Balmer et al., 2018).   Pst DC3000 infects not only its natural host but also Arabidopsis. Pst DC3000 has large repertoire of potential virulence factors, including proteinaceous effectors and polyketide phytotoxin called coronatine which structurally mimics the plant hormone JA (Xin and He 2013).

  Priming phase is induced by β-aminobutyric acid (BABA) which causes a  series of metabolic changes, characterized by a massive boost of primary metabolism through accumulation of TCAs such as citrate, fumarate, (S)-malate and 2-oxoglutarate (Pastor et al., 2014). In response to diseased plant enhanced demand for carbon can be provided by TCA intermediate through different pathways. Twenty proteinogenic amino acid can be metabolized into seven intermediates such as α-ketoglutarate, acetoacetate, acetyl-CoA, fumarate, oxaloacetate, pyruvate and succinyl-CoA  which are critical for energy generation in plants (Miflin and Habash 2002; Balmer et al., 2018). On the other hand using glutamate or using α-ketoglutarate as substrate the ϒ-aminobutyric acid (GABA) pathway produces succinate, subsequently succinate enters the TCA cycle (Li et al., 2021). GABA is a key metabolite for primary and secondary pathway and is an intermediate of nitrogen metabolism and amino acid biosynthesis. GABA can control the spread of necrotrophic fungi Botrytis (Ramos-Ruiz et al., 2019). The dual role of GABA i.e. as metabolite and as a component of signaling enables plant to resist different condition.  Another potential source to satisfy high energy demand during plant defense is the degradation of fatty acid during β-oxidation. This reaction takes place in the glyoxylate cycle that mediates the conversion of acetyl-CoA to succinate; the latter is transported from glyoxysome to the mitochondria where it is employed in TCA flux (Balmer et al., 2018). This reaction is characteristic of Arabidopsis defense responses to Pseudomonas syringae (Scheideler et al., 2002).  Carboxylic acid such as citrate one of the TCA flux intermediates is identified to play a role in metabolite signaling in yeast and animals (Wellen et al., 2009; Finkemeier et al., 2013). Study highlights that citrate and fumarate act as modifiers of transcriptional signaling during priming. Citrate pretreatment primed enhanced PR1 expression at an early stage and a PDF1.2 expression at a later stage upon PstDC3000 infection (Balmer et al., 2018). This indicates the SA signaling pathway during priming and early defense. Citrate and fumarate induce SA accumulation as early response upon PstDC3000 infection. TCA cycle intermediate fumaric acid (in tomato) and succinic acid (in A. thaliana) were accumulated in the infected leaves of both the plants indicating enhanced demand for energy (Buhtz et al., 2015).

Thionins induce pore formation on cell membranes of phytopathogens releasing potassium and calcium ions from cell. Wheat thionin accumulates in the cell walls of Fusarium inoculated plants, playing a role in controlling pathogen infection at the plant cell walls (Asano et al., 2013). Systemic plant responses including carbohydrate and nitrogen metabolism and depressed photosynthesis and respiration-related processes reflect the plasticity in adapting to pathogenic colonization. The carbohydrate metabolism to biosynthesis of aromatic compounds is linked by shikimate pathway (Herrmann and Weaver 1999).  Phosphoenolpyruvate (PEP) is utilized in the shikimate pathway, leading to the synthesis of aromatic amino acids including phenylalanine, the common substrate for lignin and flavonoid synthesis (Naoumkina et al., 2010;  Fraser and Chappel 2011). Plant defense compounds have been classified as signaling molecule, constitutive or preformed molecules, phytoanticipins and phytoalexins synthesized de novo in response to microbial attack (vanEtten et al., 1994).

References:

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