Plant Innate Immunity

Plants are infected by a huge number of pathogens of which only a few succeed in causing disease. The attack by others is responded by a sophisticated immune system possessed by the plants. Entry of phytopathogen is a vital step in causing disease. Especially in viral infection, entry is possibly through physical injuries induced either by environmental factors or by vectors like whiteflies in the case of geminivirus infection (Niehl and Heinlein 2010).

Once the virus enters in to the plant cell, it mobilizes locally and systematically through intracellular movement through the plasmodesmata. As a counter defense, plants have inbuilt immune system like microbial-associated molecular-patterns-triggered immunity (MTI) and effector-triggered immunity (ETI). MTI confers basal resistance, while ETI confers durable resistance, often resulting in hypersensitive response. Precisely, MTI involves the recognition of microbial elicitors called microbial-associated molecular patterns (MAMPs) (oligogalacturonides, ergosterol, bacterial flagellin, xylanase, chitin, cold-shock protein, cell wall fragments, peptides, and lipopolysaccharides) by a class of plasma-membrane-bound extracellular receptors called pattern recognition receptors (PRRs) (Dodds and Rathjen 2010; Beck et al. 2012) and the activation of these PRRs results in active defense responses (Hammond-Kosack and Jones 1996), which ultimately contribute to stop the progress of infection before the microbe gains a hold in the plant.

Pathogens that escapes from MTI are subjected to ETI in which pathogens ejects huge numbers of effector proteins into the cytoplasm of infected plant cells. These effector molecules are recognized by plant disease resistant (R) genes. The protein of R genes has nucleotide binding leucine repeat (NB-LRR) which bind to the effector molecules and controls the plant-pathogen interactions in a variety of host against an extensive list of pathogens (Martin et al. 2003).

In the later ETI response activates downstream MAPK cascade and WRKY transcription factors. This subsequently induces rapid transcriptional activation of a string of pathogenesis-related (PR) genes in and around the infected cell for the biosynthesis of salicylic acid (SA), jasmonic acid (JA), ethylene (ET), cell wall strengthening, lignifications, production of various antimicrobial compounds in endoplasmic reticulum and secretion into vacuoles (Iwai et al. 2006; Nomura et al. 2012; Schäfer and Eichmann 2012). Salicylic acid thus accumulated in the infected areas binds to the receptor NPR3 (NONEXPRESSOR OF PR GENES3) with low affinity and mediates the degradation of cell-death suppressor NPR1 (Fu et al. 2012), thus leading to the development of hypersensitive response (HR) (Pennell and Lamb 1997; Hayward et al. 2009). The HR is a form of programmed cell death (PCD) characterized by cytoplasmic shrinkage, chromatin condensation, mitochondrial swelling, vacuolization and chloroplast disruption (Coll et al. 2011).

Plants also possess systemic acquired resistance (SAR), which provides long-term defense against a broad-spectrum of pathogens. In addition, plants encounter the viral infection through RNA interference phenomena by utilizing small RNAs.