Translation and Host Defense Mechanisms Quiz

Physical barriers and chemical pesticides are currently used to defend against insect carriers of viruses.

The epidemiological changes caused by viral disease outbreaks, the speed with which viruses change, and the fact that viral vectors are always moving make it difficult to develop effective and long-lasting ways to fight viral diseases in plants.

Introducing plant varieties that are resistant to viral infections into commercial production is the most cost-effective technique for reducing losses caused by viral infections.

Modern biotechnologies and in-depth studies of the molecular and biochemical processes have opened up new ways to make plants’ immune systems work better against viruses.

Geminivirus IRs, but not CRISPR/Cas9-induced ORF variations, can copy and spread throughout the body without being noticed by the CRISPR/Cas9 system. This leads to differences in viral titer levels in tomato and N. benthamiana.

Mao et al. (2018) found that inhibiting RNA interference by co-expressing the TBSV P19 suppressor protein enhanced the efficacy of CRISPR/Cas9 in editing the AP1 and TT4 genes in Arabidopsis plants.

The potential consequence of employing the CRISPR/Cas9 system to target the viral genome is the development of double-strand breaks and error-prone non-homologous end joins to fix these damages, leading to the production of viral variants capable of evading the CRISPR/Cas9 recognition mechanism.

Sequence-nonspecific effects and the presence of secondary structures of dsRNA domains in sgRNA can considerably limit the editing method’s utility, as they can result in the creation of siRNAs and reduce the amount of sgRNA available for targeting viruses.

RNA interference or RNAi

Suppressor proteins can reduce DICER and RISC activity, sequester dsRNA/siRNA, and destabilize AGO proteins

The potential advantages include the requirement for only viral sequence information, the absence of the need for genetic crossing and the selection of segregating offspring, and the induction of RNA silencing by exogenous application of dsRNA

RNA-dependent RNA polymerase (RDR), suppressor of gene silencing (SGS), dicer-like (DCL), argonautes (AGO), and other proteins

CRISPR arrays store 'immune memory' of phages and plasmids in spacer sequences that intercalate between repetitions, providing a defense mechanism against future infections.

The CRISPR/Cas9 system is used to target and cleave viral or foreign plasmid DNA in plants, preventing infection by cleaving target DNA based on nucleotide complementarity using RNA-guided Cas nucleases.

Some examples include the Beet severe curly top virus, Bean yellow dwarf virus, and Cotton leaf curl Multan virus, with studies being conducted to create technologies against DNA viruses in the families Geminiviridae and Caulimoviridae.

Secondary structure-targeted guide RNAs are more effective in silencing geminiviruses like Cotton leaf curl Kokhran virus and Merremia mosaic virus compared to guide RNAs targeting the capsid protein and replicase.

Pathogen-derived resistance (PDR) proposes that a phytopathogen's genetic components expressed in plant cells can confer resistance to viral pathogenesis. This concept has significant implications for developing plant virus resistance strategies by leveraging the genetic components of phytopathogens to enhance plant immunity.

Dominant resistance genes, particularly the NB-LRR type, trigger a hypersensitive response or extreme response in infected plants. These genes activate the production of molecules such as salicylic acid, reactive oxygen species (ROS), and Ca2+ ions to defend against viral infection. Additionally, undesirable phenotypic traits associated with these genes make it difficult for plant viruses to evolve resistance to them.

The universal non-host resistance (NHR) mechanism, which includes plant defense mechanisms like the innate immune system, restricts the ability of phytoviruses to infect all plants. This mechanism involves thickening the cell wall, synthesizing secondary metabolites, and activating local necrosis to prevent pathogen entry and counter viral pathogenesis.

Recessive resistance genes interact with host cell translation factors to impede the spread of potyviruses. These genes target the viral transcript cap structure or the viral VPg protein to prevent translation, contributing to the defense against potyvirus infection within plant cells.