RNA methylation is an important regulator of RNA metabolism. The most common form of internal mRNA methylation is N6-methyladenosine (m⁶A), which is deposited by the m6A methyltransferase complex (MTC). This occurs co-transcriptionally, meaning the MTC must interact with components within the broader chromatin environment, in order to rapidly and selectively access nascent RNA. My thesis is a step towards a better understanding of those interactions. In the first part of my thesis, I examine the cellular response to UV-C irradiation, which has recently been demonstrated to induce dynamic m6A deposition. Not only do I find limited evidence to support this model, I also show this discrepancy partly arises from the cross-reactivity of m6A antibodies with poly (ADP-ribose) (PAR), which confounds imaging data. I then identify a previously uncharacterised regulatory relationship between the core MTC protein, METTL3, and the synthesis of PAR (PARylation). In the second part of the thesis, I utilise a range of experimental techniques in an attempt to describe how PARylation is affected by the loss of METTL3. These experiments give no single answer, but indicate several contexts in which PARylation and METTL3 may be linked. In the third section, I present a study of how PARP-1 and PARylation is regulated by METTL3 during the exit from pluripotency, and in the context of MEK/ERK signalling. At the heart of this section is a proteomic dataset that measures changes to the PARP-1 chromatin-associated interactome, in the presence and absence of METTL3. This identifies several interesting candidate proteins, on which further research can be based. In summary, I have identified, and begun the characterisation of, a regulatory relationship between two important processes: the m⁶A modification of RNA and PARylation. This may have important consequences for understanding several aspects of cell homeostasis and disease.