Translocation trumps receptor binding in colicin entry into Escherichia coli

Area of Science:

• Microbiology
• Molecular Biology
• Bacterial Toxin Mechanisms

Background:

• Colicin intoxication of Escherichia coli traditionally involves outer-membrane receptor binding followed by translocation.
• Receptor binding was considered a prerequisite for colicin activity and bacterial cell entry.

Purpose of the Study:

• To investigate whether colicin activity can occur independently of receptor binding.
• To identify the translocation mechanisms for colicins Ia and M, and colicin E1.
• To determine the roles of outer-membrane receptors in colicin translocation.

Main Methods:

• Construction of chimeric colicins and deletion mutants.
• Analysis of colicin activity in the absence of receptor binding.
• Investigation of translocation pathways involving specific receptors (Cir, FhuA, TolC).

Main Results:

• Colicin Ia can kill E. coli without receptor binding, utilizing a second Cir copy as a translocator.
• Colicin M can bypass receptor binding for killing, suggesting a single FhuA copy may act as both receptor and translocator.
• Colicin E1 kills E. coli independently of receptor binding through TolC translocation.

Conclusions:

• Receptor binding is not universally essential for colicin-mediated bacterial killing.
• Colicins exhibit diverse translocation mechanisms, some bypassing initial receptor interactions.
• Understanding these bypass mechanisms offers new insights into bacterial toxin delivery and potential antimicrobial strategies.