Toxic component of a type II toxin-antitoxin (TA) system, functioning in plasmid maintainence. Responsible for the post-segregational killing (PSK) of plasmid-free cells, also referred to as a plasmid addiction system. Half-life of over 2 hours. Cell killing by CcdB is accompanied by filamentation, defects in chromosome and plasmid segregation, defects in cell division, formation of anucleate cells, decreased DNA synthesis and plasmid loss. Interferes with the activity of DNA gyrase, inducing it to form a covalent GyrA-DNA complex that cannot be resolved, thus promoting breakage of plasmid and chromosomal DNA. DNA breakage requires hydrolyzable ATP. Toxicity is inhibited by labile antitoxin CcdA, which blocks the activity of CcdB; CcdA also removes bound CcdB protein from the CcdB-GyrA complex by forming a CcdA-CcdB complex, a process termed rejuvenation. Also acts to inhibit partitioning of the chromosomal DNA. Functions as a transcriptional corepressor for the ccdAB operon, repression also requires CcdA. Homodimer. Forms a complex with GyrA, probably a tetramer GyrA(2)CcdB(2), in which GyrA is inactive. Forms a complex with antitoxin CcdA; there are both high- and low-affinity binding sites for CcdA such that both CcdA-CcdB(2) and CcdA(2)CcdB(2) complexes can form. The CcdA-CcdB(2) trimer is sufficient for rejuvenation, whereas maximal operon repression occurs with CcdA(2)CcdB(2). When the CcdA:CcdB ratio is lower than 1, a CcdA(2)-CcdB(4) complex is formed which is devoid of repression activity. In this case repression is alleviated and both proteins are produced. Disruption of both ccdA and ccdB has no phenotype, except for increased plasmid loss. Belongs to the CcdB toxin family.