Critical Thinking

Plant gains a hold in the plant. Pathogens

defense mechanism

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 (Fig 1.6).

             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.

also possess systemic acquired resistance (SAR), which provides long-term
defense against a broad-spectrum of pathogens. Systemic acquired resistance
(SAR) needs endogenous accumulation of SA which results in the transcriptional
reprogramming of a battery of genes encoding PR proteins (van Loon et al. 2005;
Park et al. 2007). The SA produced in the infected site as methyl-SA (MeSA)
moves cell to cell via plasmodesmata or through the phloem to the rest of the
plant (Kiefer and Slusarenko 2003; Park et al. 2007). Once inside the plant cell,
SA binds to the high-affinity receptor NPR4 instead of binding to low-affinity
NPR3 and prevents the degradation of NPR1. This process favours cell survival
and expression of systemic immunity-related genes (Fu et al. 2012). NPR1 has
also been reported to participate in the cross talk between SA- and
JA-dependent defense pathways, thus facilitating plants to generate suitable
immune response, depending on the nature of the pathogen and the stage of
infection (Spoel et al. 2003; Koornneef and Pieterse 2008; Luna et al. 2012).

             In addition, plants can act against viral
infection by specifically degrading the viral RNA through RNA interference (RNAi)
or by gene silencing. Plants have two distinct gene silencing phenomena, namely
transcriptional gene silencing (TGS) and posttranscriptional gene silencing
(PTGS) (Al-Kaff et al. 1998; Lu et al. 2003; Padmanabhan et al. 2009; Sahu et
al. 2012a), which uses small regulating RNAs (sRNAs) to specifically target and
inactivate invading nucleic acids (Fig. 1.6) (Sharma et al. 2012).

gene silencing: The first step of PTGS is initiation in
which dsRNA is synthesized from the viral genome either by the RNA-dependent
RNA polymerase (RDR) of RNA viruses or by host RNA polymerase II in case of DNA
viruses. The dsRNA is cleaved by Dicer (DCL), an endoribonuclease (RNase)
enzyme, which generates 21-24 nt siRNA. The siRNAs are then carried to the
effector component called RNA-induced silencing complex (RISC). RISC is a
ribonucleoprotein complex with an active component termed Argonaute (AGO)
proteins, which cleave the target viral mRNA strand complementary to their
bound siRNA in the middle of siRNA–mRNA duplex. Thus, the invading viral RNAs
or the transcripts of viral DNA are eliminated through PTGS (Sharma et al.

gene silencing: DNA cytosine methylation at carbon 5 of
the pyrimidine ring 5-methylcytosine (5-meC) is a prime epigenetic event in
the defense response towards viruses (Lister et al. 2008). During RNA-directed
DNA methylation (RdDM), the production of 24-nt heterochromatic siRNA involves
Pol IV, a specialized polymerase evolved from Pol II which generates
single-stranded transcripts from the viral genome (Huang et al. 2009). These
ssRNA are converted into dsRNA by RDR2 and subsequently diced by DCL3 to
generate 24-nt siRNA. These siRNAs are incorporated into AGO4-containing
RNA-induced transcriptional silencing (RITS) complex and act as a guiding
strand for heterochromatin formation and methylation. The AGO4 imparts
chromatin modification either by cytosine methylation or by histone
methylation. In plants, it has been reported that the viral genome is targeted
for methylation through 24-nt siRNAs during infection.