The type VI secretion system (T6SS) is a molecular nanomachine which contributes to infection by injecting potent toxins via a syringe-like complex directly into host cells or competing microorganisms. Pseudomonas aeruginosa encodes three distinct T6SS machines (H1-, H2-, H3-) in separate gene clusters, which are mainly associated with Gram-negative bacterial competition. Additionally, multiple orphan gene clusters are spread throughout the genome that encode different T6SS VgrG puncturing tips and known or putative toxic effector proteins. However, the deployment of each system and mechanism of engagement of orphan gene clusters to facilitate expression and loading of a wide variety of toxic effector payloads is unknown. As the major alternative sigma factor RpoN is associated with flagella, virulence factors and cell surface control, we hypothesised that RpoN may facilitate T6SS expression control in P. aeruginosa. Using RNAseq, ChIPseq and molecular biology approaches we demonstrate that RpoN coordinates the T6SSs of P. aeruginosa, activating the H2-T6SS but repressing the H1- and H3-T6SS. Further studies showed the combined action of RpoN with a designated sigma factor activator protein Sfa2 enabled coordination of tip and effector expression to enable interbacterial killing via the H2-T6SS. Furthermore, the posttranscriptional regulator RsmA showed global coordinated repression of almost all T6SS genes. Our study further delineates the multiple regulatory mechanisms that modulate the deployment of an arsenal of T6SS effectors. This enables a versatile organism like P. aeruginosa to respond and adapt to a range of environmental conditions and competitive settings allowing it to thrive.