Toxic component of one of 6 LXG toxin-immunity modules in this strain. They promote kin selection, mediate competition in biofilms, and drive spatial segregation of different strains, indicating that LXG toxins may help avoid warfare between strains in biofilms. Mediates intercellular competition during biofilm formation; disruption of the operon disadvantages the bacteria, but overexpression of the cognate immunity protein restores growth in competition with wild-type. Overexpression alone in situ causes growth arrest but not cell lysis, a large decrease in chromosomal DNA content and the production of anucleate cells. No effect is seen on rRNA. Co-overexpression with cognate immunity protein YokJ does not cause growth arrest. The toxic effect is dependent on the epsA and tapA operons which are required for biofilm formation (PubMed:34280190). The C-terminus (residues 449-571) inhibits growth upon expression in E.coli which is neutralized by cognate immunity protein YokJ, but not by immunity proteins specific to other toxins with the LXG domain (PubMed:22200572). Probably interacts with cognate immunity protein YokJ but not with non-cognate immunity proteins. The interaction inhibits the toxic activity of YokJ (Probable). Delivery to target cells requires the type VII secretion system (T7SS) and YukE. Expressed on rich and minimal solid media likely in early stationary phase; not dependent on DegSU. Not expressed in liquid LB, but only under conditions that promote biofilm formation. Deletion of the yokI-yokJ operon has no visible growth phenotype, however it is out-competed by wild-type cells. In the N-terminal section; belongs to the LXG family. Was originally suggested to be an RNase.