Vibrio parahaemolyticus is a marine bacterium that thrives in warm climates. It is a leading cause of gastroenteritis resulting from consumption of contaminated uncooked shellfish. This bacterium harbors two putative type VI secretion systems (T6SS). T6SSs are widespread protein secretion systems found in many Gram-negative bacteria, and are often tightly regulated. For many T6SSs studied to date, the conditions and cues, as well as the regulatory mechanisms that control T6SS activity are unknown. In this study, we characterized the environmental conditions and cues that activate both V. parahaemolyticus T6SSs, and identified regulatory mechanisms that control T6SS gene expression and activity. We monitored the expression and secretion of the signature T6SS secreted proteins Hcp1 and Hcp2, and found that both T6SSs are differentially regulated by quorum sensing and surface sensing. We also showed that T6SS1 and T6SS2 require different temperature and salinity conditions to be active. Interestingly, T6SS1, which is found predominantly in clinical isolates, was most active under warm marine-like conditions. Moreover, we found that T6SS1 has anti-bacterial activity under these conditions. In addition, we identified two transcription regulators in the T6SS1 gene cluster that regulate Hcp1 expression, but are not required for immunity against self-intoxication. Further examination of environmental isolates revealed a correlation between the presence of T6SS1 and virulence of V. parahaemolyticus against other bacteria, and we also showed that different V. parahaemolyticus isolates can outcompete each other. We propose that T6SS1 and T6SS2 play different roles in the V. parahaemolyticus lifestyles, and suggest a role for T6SS1 in enhancing environmental fitness of V. parahaemolyticus in marine environments when competing for a niche in the presence of other bacterial populations.

The marine bacterium Vibrio parahaemolyticus causes gastroenteritis in humans and encodes the type III effector protein VPA0450, which contributes to host cell death caused by autophagy, cell rounding, and cell lysis. We found that VPA0450 is an inositol polyphosphate 5-phosphatase that hydrolyzed the D5 phosphate from the plasma membrane phospholipid phosphatidylinositol 4,5-bisphosphate. VPA0450 disrupted cytoskeletal binding sites on the inner surface of membranes of human cells and caused plasma membrane blebbing, which compromised membrane integrity and probably contributed to cell death by facilitating lysis. Thus, bacterial pathogens can disrupt adaptor protein-binding sites required for proper membrane and cytoskeleton dynamics by altering the homeostasis of membrane-bound inositol-signaling molecules.

The central evolutionary, ecological and paleoceanographic questions of the American tropical Neogene relate to how and during what time the Central American Isthmus formed. Geographically, closure was located between the southern edge of the Chortis Block in southern Nicaragua and the Atrato Valley in Colombia. In this region we describe, on the Caribbean side, five Neogene sedimentary basins. They are the Atrato, Chucunaque, Gatun, Bocas del Toro, and Limon Basins. On the Pacific side the Neogene sediments formed as part of the Central American Trench and are well exposed in a series of uplifted blocks on the Nicoya, Osa and Burica Peninsulas. Our analysis allows 1) a construction of the sequence of contrasting sedimentary environments which characterize the different basins, giving a composite geological history of the isthmus for the Late Neogene and 2) identifies the comparable biofacies from the different basins which allow and constrain the evolutionary and ecological questions to be posed concerning the effect of the isthmus as a biogeographic barrier. Temporally, from it's partial emergence in the Middle Miocene, the isthmus shallows by the Early Pliocene (3.5–3.4 Ma) to less than 50 m (Duque-Caro, 1990) when there is a marked differentiation of shelf marine macrobenthic species between the Caribbean and the Pacific. The evidence from reliably dated, large, diverse exchanges of North and South American vertebrates on land constrains the final closure date to not later than 2.8–2.5 Ma (Marshall, 1988). Given that no conclusive evidence for final closure can come exclusively from a study of sedimentary facies, when depths of less than 50 m are involved, the present window of almost 1 Ma, during which final closure must have occurred, will only be narrowed further by the detailed study of very shallow-water fossil clades and complementary molecular data. Present studies indicate that such clades are abundantly preserved.