Calcium ions (Ca²⁺) are ubiquitous signaling molecules that play critical roles across all domains of life. In plants, Ca²⁺ acts as a central second messenger that transduces a wide array of biotic and abiotic signals, including those triggered during interactions with microbial pathogens. Upon pathogen recognition, plants often exhibit rapid and localized Ca²⁺ influxes that initiate downstream immune responses. However, the role of Ca²⁺ is not restricted to the host; many bacterial pathogens have evolved mechanisms to sense and respond to environmental Ca²⁺ levels, using these signals to fine-tune their physiology and coordinate virulence.Pseudomonas syringae, a model bacterial plant pathogen, uses a sophisticated arsenal of virulence factors, including the type III secretion system (T3SS), virulence factors, and phytotoxins, to manipulate plant cellular processes and suppress immunity. Emerging evidence suggests that Ca²⁺ serves as an important environmental cue that modulates the expression and activity of these virulence determinants. Despite this, the molecular mechanisms by which Ca²⁺ regulates bacterial pathogenicity, and the ecological consequences of such regulation, remain poorly understood. In Chapter 2, I characterized cynT, which encodes for a β-class carbonic anhydrase, by comparative transcriptomics. The transcriptomics analysis across different media and conditions supplemented with calcium revealed that cynT influences the expression of virulence and metabolic genes in a context-dependent manner, and deletion of cynT impact phenotypes of P. syringae. In Chapter 3, I investigated the srfABC operon, which was found to be regulated by cynT. Functional assays revealed that srfABC contributes to both virulence and interbacterial competition. Analysis of SrfA indicated it is secreted by P.syringae in a T3- and T6- independent manner. In Chapter 4, I explored how calcium modulates the activity of type VI secretion system (T6SS)-dependent competition. I found that calcium enhances T6SS-mediated killing against E.coli. Further analyses implicated GacAS plays a key role in integrating calcium signals to modulate T6SS activity. By dissecting the regulatory networks and physiological outcomes linked to Ca²⁺ sensing, this work provides new insights into how bacterial pathogens exploit host and environmental cues to establish infection and outcompete microbial rivals. These findings underscore the importance of calcium as an environmental signal shaping both virulence and microbial interactions in plant-associated bacteria.