Abstract
We are fortunate to possess a wealth of knowledge regarding the primary intracellular targets of antibiotics and strong clinical appreciation for the viability-compromising effects of target inhibition by these remarkable chemical entities1. It is not by coincidence that antibiotic lethality is almost exclusively initialized in bacterial cells through the arrest of fundamental processes, i.e. DNA replication, RNA transcription, protein translation and cell wall biosynthesis. Yet the question of how antibiotics ultimately kill bacteria remains a quintessential ‘black box’ problem. Despite the ubiquity of their usage, our understanding of the specific events that connect drug-target interactions with antibiotic-mediated cell death, including the cell death process, remains incomplete.
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