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Protein export pathways are important for bacterial physiology among pathogens and non-pathogens alike. This includes the Twin-Arginine Translocation (Tat) pathway, which transports fully folded proteins across the bacterial cytoplasmic membrane. Some Tat substrates are virulence factors, while others are important for cellular processes like peptidoglycan remodeling. Some bacteria encode more than one copy of each Tat component, including the Gram-negative soil isolate Acinetobacter baylyi. One of these Tat pathways is essential for growth, while the other is not. We constructed a loss-of-function mutation to disrupt the non-essential tatC2 gene and assessed its contribution to cell growth under different environmental conditions. While the tatC2 mutant grew well under standard laboratory conditions, it displayed a growth defect and an aberrant cellular morphology when subjected to high temperature stress including an aberrant cellular morphology. Furthermore, increased sensitivities to detergent suggested a compromised cell envelope. Lastly, using an in vitro co-culture system, we demonstrate that the non-essential Tat pathway provides a growth advantage. The findings of this study establish the importance of the non-essential Tat pathway for optimal growth of A. baylyi in stressful environmental conditions. 

Directing the flow of protein traffic is a critical task faced by all cellular organisms. In Gram-negative bacteria, this traffic includes lipoproteins. Lipoproteins are synthesized as precursors in the cytoplasm and receive their acyl modifications upon export across the inner membrane. The third and final acyl chain is added by Lnt, which until recently was thought to be essential in all Gram-negatives. In this report, we show that Acinetobacter species can also tolerate a complete loss-of-function mutation in lnt. Absence of a fully functional Lnt impairs modification of lipoproteins, increases outer membrane permeability and susceptibility to antibiotics, and alters normal cellular morphology. In addition, we show that loss of lnt triggers a global transcriptional response to this added cellular stress. Taken together, our findings provide new insights on and support the growing revisions to the Gram-negative lipoprotein biogenesis paradigm.