Programming and reprogramming requires changes in gene expression regulated via transcription and mRNA decay in response to developmental and environmental cues. Evolutionarily conserved PAT1 proteins activate mRNA decapping which initiates 5’ to 3’ decay. Arabidopsis encodes 3 PAT proteins: PAT1, PATH1 and PATH2. PAT1 is under the surveillance by the Resistance protein SUMM2, and pat1 loss-of-function triggers autoimmunity. To block autoimmunity in pat1, I generated pat single, double and triple mutants in the summ2 background using CRSPR/CAS9 and studied mRNA decay in these mutants. I show that all 3 PAT paralogs are required for decapping selected mRNAs in complexes with the decapping component LSM1. Transcriptome profiling revealed that mRNA of the ASL9 transcription factor specifically accumulates in pat triple mutants. In addition, capped ASL9 mRNAs accumulate in dark-grown seedlings of pat triple mutants exposed to ethylene while they are degraded in wild type controls. Moreover, pat triple mutants and transgenic plants overexpressing ASL9 are unable to develop lateral roots and seedling apical hooks. RNA immunoprecipitation (RIP) assays indicated that PAT1 and PATH2 are primarily involved in targeting ASL9 transcripts, while localization studies suggest PATH1 may serve a similar function in the absence of the other two PATs. Thus PAT proteins mediate developmental programming and reprogramming, and ASL9 transcripts are decay targets which need to be removed to allow formation of lateral roots and apical hooks. In addition to functions of mRNA decay in regulating developmental processes, I describe a specific function of PAT1 mediated decay in response to ABA and drought stress. Only pat1 mutants exhibit hypersensitivity to ABA and ABA-responsive genes, rather than ABA biosynthesis genes, persist longer in pat1 mutants. I observed increased tolerance to drought stress and resistance to Pythium irregulare in pat1 mutants, possibly due to PAT1 specifically decapping transcripts of the canonical ABA-responsive gene COR15A. I also studied the function of mRNA decay factors in responses to Turnip mosaic virus (TuMV) which infects many plant species. Recent research has found that the mRNA decay components DCP2, XRN4 and VCS have diverse functions in viral infection. Here I report that the mRNA decapping components LSM1 and PATs function differently from DCP2 and DHH1 and are essential for TuMV infection. Furthermore, TuMV interferes with their decapping functions and recruits them with TuMV CP, probably for viral assembly.This thesis comprises an introduction to mRNA decay and to plant innate immunity with special focus on autoimmunity, plant developmental processes including LR and apical hook formation, osmotic stress responses including ABA signalling, and the infection cycle of TuMV. The results10are presented in three manuscripts. The first, “PAT mRNA decay factors target ASL9 transcripts to enable apical hook and lateral root development”, links mRNA decay with developmental programming and reprogramming. The second, “AtPAT1 mRNA decay factor functions in osmotic stress responses through decapping ABA responsive genes”, links mRNA decay with ABA signalling in response to osmotic stress. The third, “TuMV interferes with PATs and LSM1 decapping components for viral infection”, links mRNA decay with TuMV infection.