RNA processing steps that regulate plant immune responses. Pathogen associated molecular patterns (PAMPs) are recognized by pathogen recognition receptors (PRRs), which induce signaling cascades and lead to PAMP triggered immunity (PTI). To overcome this, bacterial, oomycete or fungal pathogens release effector molecules that inhibit PTI; this leads to effector-triggered susceptibility (ETS). Plants have evolved Resistance (R) proteins that recognize the effectors and lead to effector-triggered immunity (ETI). PTI and ETI both trigger downstream defence gene activation followed by RNA processing steps that include 3′ polyadenylation, splicing, 5′ capping and mRNA export. MAC5A/B associate with the MOS4-associated Complex (MAC), which associates with the spliceosome; therefore, MAC5A/B may contribute to mRNA splicing during pathogen defence [2]. MOS11 is also found in the nucleus; however, it is involved with mRNA export [3]. DCL2 and DCL4 are both required in the formation of siRNAs in RNAi, which assists in plant immunity [4, 5]. Similarly, AGO1, AGO2, and AGO7 are involved in RNAi, they are RNA-binding components of the RISC, which recruits the target mRNA [5, 6].
