Editing Arabidopsis thaliana (section)

===Evolutionary aspect of plant-pathogen resistance===
Plants are affected by multiple [[pathogens]] throughout their lifetimes. In response to the presence of pathogens, plants have evolved receptors on their cell surfaces to detect and respond to pathogens.<ref name="Bent1994">{{cite journal |vauthors=Bent AF, Kunkel BN, Dahlbeck D, Brown KL, Schmidt R, Giraudat J, Leung J, [[Brian Staskawicz|Staskawicz BJ]] |title=RPS2 of ''Arabidopsis thaliana'': a leucine-rich repeat class of plant disease resistance genes |journal=Science |volume=265 |issue=5180 |pages=1856–60 |date=September 1994 |pmid=8091210 |doi=10.1126/science.8091210 |bibcode=1994Sci...265.1856B}}</ref> ''Arabidopsis thaliana'' is a model organism used to determine specific defense mechanisms of plant-pathogen resistance.<ref name="Zipfel, C. 2004">{{cite journal |vauthors=Zipfel C, Robatzek S, Navarro L, Oakeley EJ, Jones JD, Felix G, Boller T |title=Bacterial disease resistance in Arabidopsis through flagellin perception |journal=Nature |volume=428 |issue=6984 |pages=764–7 |date=April 2004 |pmid=15085136 |doi=10.1038/nature02485 |bibcode=2004Natur.428..764Z |s2cid=4332562}}</ref> These plants have special receptors on their cell surfaces that allow for detection of pathogens and initiate mechanisms to inhibit pathogen growth.<ref name="Zipfel, C. 2004"/> They contain two receptors, FLS2 (bacterial flagellin receptor) and EF-Tu (bacterial EF-Tu protein), which use signal transduction pathways to initiate the disease response pathway.<ref name="Zipfel, C. 2004"/> The pathway leads to the recognition of the pathogen causing the infected cells to undergo cell death to stop the spread of the pathogen.<ref name="Zipfel, C. 2004"/> Plants with FLS2 and EF-Tu receptors have shown to have increased fitness in the population.<ref name="Delaney, T. 1994"/> This has led to the belief that plant-pathogen resistance is an evolutionary mechanism that has built up over generations to respond to dynamic environments, such as increased predation and extreme temperatures.<ref name="Delaney, T. 1994"/>

''A. thaliana'' has also been used to study SAR.<ref name="Lawton, K. 1996">{{cite journal |vauthors=Lawton K, Friedrich L, Hunt M |year=1996 |title=Benzothiadizaole induces disease resistance by a citation of the systemic acquired resistance signal transduction pathway |journal=The Plant Journal |volume=10 |issue=1 |pages=71–82 |doi=10.1046/j.1365-313x.1996.10010071.x |pmid=8758979 |doi-access=free}}</ref>
This pathway uses benzothiadiazol, a chemical inducer, to induce transcription factors, mRNA, of SAR genes. This accumulation of transcription factors leads to inhibition of pathogen-related genes.<ref name="Lawton, K. 1996"/>

Plant-pathogen interactions are important for an understanding of how plants have evolved to combat different types of pathogens that may affect them.<ref name="Delaney, T. 1994"/> Variation in resistance of plants across populations is due to variation in environmental factors. Plants that have evolved resistance, whether it be the general variation or the SAR variation, have been able to live longer and hold off necrosis of their tissue (premature death of cells), which leads to better adaptation and fitness for populations that are in rapidly changing environments.<ref name="Delaney, T. 1994"/> In the future, comparisons of the [[pathosystem]]s of wild populations + their [[coevolution|coevolved]] pathogens with wild-wild hybrids of known parentage may reveal new mechanisms of [[balancing selection]]. In [[life history theory]] we may find that ''A. thaliana'' maintains certain alleles due to [[pleitropy]] between plant-pathogen effects and other traits, as in livestock.<ref name="Fridman-2015">{{cite journal |last=Fridman |first=Eyal |title=Consequences of hybridization and heterozygosity on plant vigor and phenotypic stability |journal=[[Plant Science (journal)|Plant Science]] |publisher=[[Elsevier]] |volume=232 |year=2015 |issn=0168-9452 |doi=10.1016/j.plantsci.2014.11.014 |pages=35–40 |pmid=25617321|bibcode=2015PlnSc.232...35F }}</ref>

{{anchor|EDS1 family|CCHELO|EDS1|PAD4}}Research in ''A. thaliana'' suggests that the [[EDS1 family|immunity regulator protein family EDS1]] in general co-evolved with the [[CCHELO|CC{{sub|HELO}}]] family of [[NOD-like receptor|nucleotide-binding{{ndash}}leucine-rich-repeat-receptors (NLRs)]]. Xiao et al. 2005 have shown that the [[powdery mildew]] immunity mediated by ''A. thaliana''{{'}}s [[RPW8]] (which has a CC{{sub|HELO}} [[protein domain|domain]]) is dependent on two members of this family: ''[[EDS1]]'' itself and ''[[PAD4]]''.<ref name="Lapin-et-al-2020">{{cite journal |last1=Lapin |first1=Dmitry |last2=Bhandari |first2=Deepak D. |last3=Parker |first3=Jane E. |title=Origins and Immunity Networking Functions of EDS1 Family Proteins |journal=[[Annual Review of Phytopathology]] |publisher=[[Annual Reviews (publisher)|Annual Reviews]] |volume=58 |issue=1 |date=2020-08-25 |issn=0066-4286 |doi=10.1146/annurev-phyto-010820-012840 |pages=253–276 |s2cid=218617308 |pmid=32396762 |hdl=1874/413668}}</ref>

{{anchor|RPS5|RESISTANCE TO PSEUDOMONAS SYRINGAE 5|PBS1|AvrPphB SUSCEPTIBLE 1}}''[[RESISTANCE TO PSEUDOMONAS SYRINGAE 5]]/RPS5'' is a [[plant disease resistance protein|disease resistance protein]] which guards ''[[AvrPphB SUSCEPTIBLE 1]]/PBS1''. ''PBS1'', as the name would suggest, is the target of ''[[AvrPphB]]'', an [[effector (biology)|effector]] produced by [[Pseudomonas syringae pv. phaseolicola|''Pseudomonas syringae'' pv. ''phaseolicola'']].<ref name="Pottinger-Innes-2020">{{cite journal |last1=Pottinger |first1=Sarah E. |last2=Innes |first2=Roger W. |title=RPS5-Mediated Disease Resistance: Fundamental Insights and Translational Applications |journal=[[Annual Review of Phytopathology]] |publisher=[[Annual Reviews (publisher)|Annual Reviews]] |volume=58 |issue=1 |date=2020-08-25 |issn=0066-4286 |doi=10.1146/annurev-phyto-010820-012733 |pages=139–160 |pmid=32284014 |s2cid=215757180|doi-access=free }}</ref>