R gene

Plant defense mechanisms depend on detection of fungal and bacterial pathogens. R proteins are a way of identifying the pathogen effectors and stopping the infection. Molecules essential for pathogen defense are pattern recognition receptors (PRRs), wall associated kinase (WAKs), receptors with nucleotide-binding domain (NLRs) and leucine-rich repeats (LRRs). All these R proteins play roles in detecting and recognizing pathogen effectors, initiating multiple signal transductions inside the plant cell, these signals transductions will lead to different responses that will aid in pathogen destruction and prevention of further infection. These responses are: • Production of Reactive Oxygen (ROS) • Hypersensitive Response • Closure of the stomata • Production of different chemical compounds (terpenes, phenolic, tannins, alkaloids, phytoalexins) Note that plants have various mechanisms to prevent and detect pathogenic infections, but factors such as geography, environment, genetic, and timing can affect the recognition pattern of a pathogen or can have an effect on the recognition of avirulent (avr) pathogens in plants. ==Pathogen recognition==

R genes synthesize proteins that will aid with the recognition of pathogenic effectors: Pattern recognition receptors (PRRs) This receptor is often composed of leucine-rich repeats (LRRs). LRRs have a wide range of bacterial (proteins), fungal (carbohydrates) and virulent (nucleic acids) recognition, this means that LRRs recognizes many different molecules but each LRRs usually has a very specific molecule it detects. The ability of PRRs to recognize various pathogenic components relies on a regulatory protein called brassinosteroid insensitive 1 –associated receptor kinase (BAK1). Once the pathogen has been recognized by PRRs the release of a kinase into the nucleus has been transduced triggering a transcriptional reprogramming. Wall associated kinase (WAKs) The plant cell wall is conformed of pectin and other molecules. Pectin has abundant galacturonic acids which is the compound that WAKs recognizes after a foreign invasion in the plant. Every WAKs (WAK1 & WAK2) has an N-terminal which interacts with pectin in the cell wall when pectin is being degraded to galacturonic acids by fungal enzymes. Pathogen-associated molecular pattern (PAMPs) and damage-associated molecular pattern (DAMPs) are often identified by lectins which is a protein that binds specific carbohydrates. Nucleotide-binding domain and leucine-rich repeats (NLRs) Most R genes code for these immune receptor proteins. ==Signal transduction==

A plant defense has two different types of immune system, the one that recognizes pathogen/microbes associated molecular patterns (PAMPs), and this is also known as PAMP-triggered immunity (PTI). Plant defense mechanism depends on immune receptors found on the plasma membrane and then the mechanism can sense the pathogen associated molecular patterns (PAMPs) and microbial associated molecular patterns (MAMPs). Detection of PAMPs triggers a physiological change in the cell activated by the pattern recognition receptors (PRRs) initiating a cascade response which through the recognition of PAMPs and MAMPs lead to the plant resistance. The other type of defense is also known as effector-triggered immunity (ETI) which is the second type of defense mediated by R-proteins by detecting photogenic effectors. ETI detects pathogenic factors and initiates a defense response. ETI is a much faster and amplified system than PTI and it develops onto the hypersensitive response (HR) leading the infected host cell to apoptosis. This does not terminate the pathogen cycle, it just slows the cycle down. Plants have many ways of identifying symbiotic or foreign pathogens; one of these receptors causes fluctuations in the calcium ions and this fluctuation in the calcium ions. A transcription factor plays an important role in defenses against pathogenic invasion. ==Pathogen invasion==

Despite the sophiscation of plant defenses, some pathogens have evolved ways to overcome these defenses in order to infect and spread. Pathogen elicitors are molecules that stimulate any plant defense; among these elicitors we can find two types of pathogen derived elicitors, pathogen/microbe associated molecular pattern (PAMPs/MAMPs), and also there is a second type which is produced by plants known as damage or danger associated molecular patterns (DAMPs). PTI is a way of responding against pathogen actions happening outside the cell, but a much stronger response like ETI is generated in response to effectors molecules. Once there is an induced resistance also known as priming, the plant can react faster and stronger to a pathogen attack. A known priming inducer is called β-aminobutyric acid (BABA) which is a non-protein amino acid. Successful pathogens evolve changes in their chemical conformation in order to avoid detection by PRRs and WAKs. Some viruses have mechanisms that allow them to avoid or suppress the RNA-mediated defense (RMD) that some viruses induce in non-transgenic plants. Further studies have shown that this suppression of the host defense has been done by HC-protease (HCPro) encoded in the Potyviral genome. It was later stablished that HCPro was a mechanism used to suppress post-transcriptional gene slicing (PTGs). Cucumber mosaic virus (CMV) uses a different protein called 2b () which is also a suppressor of PTGS in Nicotiana benthamiana. Even though HcPro and the 2b protein have different protein sequence specific to their own virus, both target the same instrument of defense through different mechanisms. ==Genetic engineering==

R genes are common subjects of gene cloning. Every advance in techniques of sequencing and transfer has eased this process, progressively requiring less linkage drag, expense, and laboratory work over time. In the future even better results are expected from ever larger data sets, across ever larger numbers of individuals and populations, with ever greater resolution due to both more accurate sequencing and post-sequencing computational comparison between individuals. == See also ==