RecA influences biofilm development in the opportunistic pathogen Acinetobacter baumannii

Acinetobacter baumannii, a Gram-negative opportunistic pathogen, is a leading cause of hospital-acquired infections. A. baumannii is difficult to eradicate from hospitals due to its propensity to quickly gain antibiotic resistances and ability to robustly survive on dry surfaces. These strategies are largely mediated by mutagenesis and biofilm development, respectively. Mutagenesis is partly governed by the DNA damage response (DDR). Biofilms are multicellular communities, often surface-attached, that are more difficult to eradicate than free-living planktonic cells. There is increasing evidence that the DDR and biofilm development are linked processes. Here, we show that upon DNA damage, the relative intracellular concentration of RecA, the key DDR protein, is lower than those of Escherichia coli. Notably, we report that RecA negatively influences biofilm development. Cells lacking RecA ({Delta}recA), that are unable to upregulate the DDR, have increased surface attachment and sugar content within the biofilm matrix. We further show that in A. baumannii, a modest increase in RecA concentrations, akin to DDR induction, decreases surface-attachment. Importantly, biofilms formed by {Delta}recA cells are more difficult to eradicate with antibiotic treatment. The evidence suggests that the A. baumannii DDR influences survival independent from mutagenesis. It also demonstrates the importance of understanding fundamental biology to better appreciate the relationships between different bacterial survival strategies.