Type VI Secretion System Facilitates Intraspecies Killing in Vibrio vulnificus via the Associated rhs Toxin/Antitoxin System


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Vibrio vulnificus is a human pathogen that causes both gastrointestinal symptoms and blistering skin lesions. According to the United States Center for Disease Control and Prevention (CDC), one in every five people with a V. vulnificus infection die, often very quickly. Most of the infections are transmitted by eating raw shellfish, particularly molluscan shellfish such as oysters, that are colonized with these pathogenic bacteria. Oysters become colonized with Vibrio by feeding on marine aggregates that contain these bacteria. Multiple strains of V. vulnificus colonize onto the surface area of the oyster matrices through the oyster's filter feeding process. These bacteria possess many effector molecules that are secreted using many of the secretion systems that are present in gram negative bacteria, including the Type VI Secretion System (T6SS). The T6SS plays a large role in the pathogenicity of many gram-negative bacteria [1]. The T6SS in V. vulnificus is a syringe-like apparatus that injects effector proteins into neighboring prokaryotic cells. There are two different types of the T6SS in V. vulnificus, Type I (T6SS1) and Type II (T6SS2). T6SS2 has been found in many species of bacteria but the T6SS1 has only been found in a handful. For instance, most V. vulnificus strains contain the T6SS2 but very few encode for the T6SS1. However, both T6SS1 and T6SS2 remain largely ambiguous in V. vulnificus. The T6SS1 has been previously shown to be active, and here we present evidence that T6SS2 is also able to cause intraspecies killing in V. vulnificus. This potentially provides an advantage for some strains of V. vulnificus when competing with other strains for space and nutrients in an environment where surface area is limited, such as an oyster. A competition assay was used to determine the effectiveness of the T6SS2 in V. vulnificus to study strain-to-strain intraspecies killing. We found that some strains of V. vulnificus significantly out-competed other strains in vitro. V. vulnificus MO6 outcompeted V. vulnificus JY1701, most likely due to the effector proteins or toxins that are being secreted through the T6SS2. Here, we propose the cellular mechanisms that provide these competitive advantages in the strain-to-strain intraspecies competition observed when V. vulnificus integrates into marine aggregates.