Biotic interactions

Prior exposure to biotic stresses has been reported to have improved the defense response of plants. Studies on this topic have a similar bias towards Arabidopsis and cultivated plants as studies on abiotic stress. Reviews by Alonso et al. (2018) and Mauch-Mani et al. (2017) combined the information on biotic interactions and the epigenetic contribution in the response for several plant species (Alonso, Ramos‐Cruz et al. 2019; Mauch-Mani et al. 2017).‌

In the natural environment, plants encounter biotic stress like the occurrence of herbivores, parasites, and pathogens, or the absence of symbiotic partners, and competition with other plants, and hence plant defense response has coevolved with the evolution of interacting species and consequently developed diverse strategies of plant defense mechanisms (Karban et al. 1999; Holeski et al. 2012). These strategies have provided plant fitness benefits against stressors, e.g., herbivore damage (Baldwin et al. 1998). Priming and somatic memory to stress, like the exposure to a pathogen, has been repeatedly reported in correlation with epigenetic changes (Lämke and Bäurle 2017). The task for the future, as the authors note, is to overcome "correlation" and test causation. In other words, it is yet unresolved if these epigenetic changes are actively involved in the priming response. However, a notable study by Yu et al. (2013) demonstrated that treating Arabidopsis thaliana with a peptide of bacterial origin induced the active demethylation of transposable elements (TE), which mobilized short-interfering RNAs/siRNAs and led to the transcriptional activation of genes involved in the defense against bacteria (Yu et al. 2013). The study further found that DNA demethylation negatively affected the growth of a bacterial pathogen, suggesting a close link between the two.

Table 2: List of epigenetic modification reported for biotic stress:

Components	Stress	Species	Function	References	Type of plasticity
DNA methylation	Bacterial infection, chemical stressors	A. thaliana	PR1 Promotor	Slaughter et al. 2012	Intra-generational
DNA methylation	Bacterial pathogen, avirulent bacteria, or	A. thaliana	Constitutively overexpress PR1	Dowen et al. 2012	Trans-generational
DNA methylation	Bacterial pathogen Pseudomonas syringae	A. thaliana	Basal- and/or flg22-induced expression of several MAMP-responsive NLRs was enhanced	Yu et al. 2013	Intra-generational
H3K27me3,DNA methylation	Bacterial infection	A. thaliana	DNA methylation	Luna et al. 2012	Trans-generational
DNA methylation	Tobacco mosaic virus (TMV)	Tobacco	Hypomethylation at the NtAlix1 locus	Wada et al. 2004	Intra-generational
DNA methylation	RNA virus	Tomato	SiRNA-mediated methylation	Bian et al. 2006	Intragenerational
RNA silencing/DNA methylation	Cucumber mosaic virus (CMV)‐	Petunia	Targeting dsRNA to the promoter,	Kanazawa et al. 2011	Trans-generational
DNA methylation	Caterpillar herbivory	A. thaliana & Tomato	NRPD2A, NRPD2B,DCL2/DCL3/DCL4	Rasmann et al. 2012	Trans-generational
Small RNA	Leaves treated with bacterial flagellin 22	A. thaliana	MiR393 that negatively regulates messenger RNAs for the F-box auxin receptors TIR1, AFB2, and AFB3, flagellin increases resistance to the bacterum	Navarro et al. 2006	no information
chromatin Remodeling	Pseudomonas syringae infection	A. thaliana	SNI1 (SUPRESSOR OF NPR1, INDUCIBLE)	Durrant, Wang, and Dong 2007
histone methylation	Pseudomonas syringae infection	A. thaliana	EMBRYONIC FLOWER 1 and 2	Kim, Zhu, and Renee Sung 2010	Intragenerational
histone methylation	A. brassicicola and B. cinerea infections	A. thaliana	Histone methyltransferase SET DOMAIN GROUP8	Berr et al. 2010	trans-generational
histone deacetylation	Pseudomonas syringae infection	A. thaliana	HDA19	Choi et al. 2012