In response to external stimuli plants are in a constant balancing act, ultimately accessing the instructions within their genetic material to respond. The response is transcribed into transiently lived RNA molecules, carrying messages to be translated into functional proteins or directly acting as regulatory agents or enzymatically. Although short-lived, these RNA transcripts are tightly regulated through many different mechanisms of post-transcriptional control. The discovery and annotation of chemical modifications, moieties that can be added to the canonical bases of RNA, is one such mechanism of post-transcriptional regulation. With our understanding of the diversity of modifications, their presence in various RNA species, and their effects on individual transcripts and global population increases, it is clear that they are essential for the proper functioning of RNA transcripts in plants. In my dissertation work, I examine how the presence of the RNA modification N6- methyladenosine in RNA transcripts effects RNA abundance, stability, and ultimately resistance and response to pathogenesis in the model plant Arabidopsis thaliana. Utilizing biochemical, genetic, and bioinformatic approaches, I characterize the post-transcriptional regulation of N6- methyladenosine before and during pathogen infection. I first examine how global alteration in RNA modification effect the preparedness and reactivity to pathogen exposure, describing a significant robustness in plants with decreased levels of modification to multiple pathovars. I then examine the epi-transcriptomic profile of N6-methyladenosine before and after infection, describing a strategic coordination of modification deposition and removal on transcripts directly involved in balancing stress response and basal growth and development, prior to and in response to pathogen exposure. Next, I examine the relationship between N6-methyladenosine and cleavage and degradation of transcripts, describing a condition-specific model whereby the global effects of modification on transcript cleavage and stability shift in response to infection. Then I present data supporting a model whereby N6-methyladenosine presence is controlled by the upregulation of known eraser protein ALKBH10B during pathogen stress, preferentially erasing modifications with regional specificity across target transcripts. Further, I present a catalogue of mutant lines targeting the three most abundant N6-methyladenosine eraser proteins, ALKBH10B, ALKBH9C, and ALKBH9B and characterize their expression patterns as well as their phenotypes related to growth and development. I confirm previous findings and present novel phenotypes related to each ALKBH protein. Continuing, I present preliminary data showing the localization and protein interactions of two of the nuclear eraser proteins, ALKBH10B and ALKBH9C in Arabidopsis, and enrichment across chromatin of Arabidopsis N6-methyladenosine writer MTA suggesting a co-transcriptional model for both N6-methyladenosine writing and erasing in Arabidopsis. Finally, I present the establishment of a pipeline and protocol using Oxford Nanopore Technologies Direct RNA sequencing that allows the capture of nascently forming chromatin associated RNA and the RNA modifications which they harbor. Utilizing a combination of genomic, molecular, and genetic analyses, these studies contribute to our understanding of the regulation of the epitranscriptome and the mechanisms by which it is regulated in a plant system and open important research questions for future study.