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Review discusses how DNA damage response influences biofilm behavior in Acinetobacter baumannii, highlighting its significance in infection persistence.
Acinetobacter baumannii is a clinically significant pathogen that is difficult to eliminate from infected individuals; indeed, infections due to this organism cost the health care system tens of millions of dollars per year. This pathogen readily infects immunocompromised individuals and can survive extreme conditions, including the osmotic and immune stresses of the human host and prolonged desiccation on hospital surfaces. The survival success of A. baumannii is in large part due to the formation of multicellular communities, or biofilms, that afford cells protection from external stresses, such as antibiotics and desiccation. Cells within biofilms cycle between a surface-attached, protected state and dispersal, in which they egress the biofilm and disseminate to new niches while becoming vulnerable to antibiotics and host immunity. The fate decision to either stay or leave the biofilm is just beginning to be understood in A. baumannii , and we review the current state of knowledge here. Emerging evidence suggests that the DNA damage response (DDR), and specifically the RecA protein, is key to orchestrating this decision.
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Nguyen et al. (2026) studied this question.
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