Plants are infected by a large number of pathogens, only a few of which are successful in causing disease. Attack by others is responded to by a sophisticated immune system that plants possess. Entry of plant pathogens is a vital step in causing disease. Particularly in the case of viral infection, entry is likely through physical injuries induced either by environmental factors or by vectors such as whiteflies in the case of geminivirus infection (Niehl and Heinlein 2010). . Say no to plagiarism. Get a tailor-made essay on “Why Violent Video Games Should Not Be Banned”? Get the original essay Once the virus enters the plant cell, it mobilizes locally and systematically by intracellular movement through the plasmodesmata. As a counterdefense, plants have a built-in immune system, such as microbial-associated molecular pattern-triggered immunity (MTI) and effector-triggered immunity (ETI). MTI confers basal resistance, while ETI confers long-lasting resistance, often resulting in a hypersensitive response. Specifically, MTI involves the recognition of microbial elicitors called microbe-associated molecular patterns (MAMPs) (oligogalacturonides, ergosterol, bacterial flagellin, xylanase, chitin, cold shock protein, cell wall fragments, peptides, and lipopolysaccharides) by a class of plasma- extracellular membrane-bound receptors called pattern recognition receptors (PRRs) (Dodds and Rathjen 2010; Beck et al. 2012) and activation of these PRRs results in active defense responses (Hammond-Kosack and Jones 1996 ), which ultimately help stop the progression of the infection before the microbe takes hold in the plant. Pathogens that escape from MTI are subjected to ETI in which pathogens eject large numbers of effector proteins into the cytoplasm of infected plant cells. These effector molecules are recognized by plant disease resistance (R) genes. The R genes protein has a nucleotide-binding leucine repeat (NB-LRR) that binds effector molecules and controls plant-pathogen interactions in a variety of hosts against a long list of pathogens (Martin et al. 2003). The ETI response activates the downstream MAPK cascade and WRKY transcription factors. This then induces rapid transcriptional activation of a chain 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, lignification, production of various antimicrobial compounds in the endoplasmic reticulum and secretion into vacuoles (Iwai et al. 2006; Nomura et al. 2012; Schäfer and Eichmann 2012). The salicylic acid thus accumulated in infected areas binds to the NPR3 (NONEXPRESSOR OF PR GENES3) receptor with low affinity and mediates the degradation of the cell death suppressor NPR1 (Fu et al. 2012), thus leading to the development of a hypersensitive response (HR) (Pennell and Lamb 1997; Hayward et al. 2009). 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). Keep in mind: this is just a sample. Get a custom paper now from our expert writers.Get a custom essayPlants also possess systemic acquired resistance (SAR), which provides long-term defense against a broad spectrum of pathogens. In addition, plants..