How plants integrate and respond to multiple simultaneous or consecutive stresses is an increasingly pressing question with the advent of Climate Change. Presented in this Ph.D. thesis is an exploration of the crosstalk between hypoxia and immune responses and the role of the N-degron pathway in its regulation. Transcriptomic analyses using RNA-Seq facilitated dissection of Arabidopsis responses to combined hypoxia and flg22, uncovering interactions between responses to these stresses. It was discovered that hypoxia represses flg22-induced responses at the gene level and also dampens cellular immune responses (e.g. MAPK signalling and callose deposition). This work also found combined hypoxia/flg22 treatments induce novel responses which may point towards pathways that antagonise multi-stress resistance but also those which lie at the intersection of multiple stresses. One pathway which was particularly enriched under combined treatments was jasmonic acid (JA) signalling. The phytohormone JA is well known for its involvement in plant stress responses and this study further highlighted its role as a potential point of intersection for hypoxia and flg22 responses. Further, a potential role for the N-degron pathway in the removal of repression of JA signalling by the repressor protein, JASMONATE ZIM-DOMAIN 8 (JAZ8), was proposed by this work, with an N-degron pathway component, ARGINYL-TRANSFERASE 1 (ATE1), binding JAZ8 and mediating its destabilization. This further supports JA as a point of crosstalk between hypoxia and flg22 responses with the N-degron pathway potentially playing a regulatory role. Similar work to that in plants was attempted in mammals to allow direct comparison of conserved roles of the N-degron pathway in innate immunity and its role in the interplay between hypoxia and immunity. Aims to generate ATE1 knockout RAW264.7 macrophages were however unsuccessful, halting this work.