Models and Nomenclature for Cytoplasmic Incompatibility: Caution over Premature Conclusions
Shropshire, J. D.†, Leigh, B., Bordenstein, S. R., Duplouy, A., Riegler, M., Brownlie, J. C., & Bordenstein, S. R.† (2019). Models and Nomenclature for Cytoplasmic Incompatibility: Caution over Premature Conclusions-A Response to Beckmann et al. Trends in genetics: TIG.
Recent studies have identified two genes in bacteriophage WO, cifA and cifB, that contribute to the induction of cytoplasmic incompatibility (CI), and one of these two genes, cifA, rescues it. These findings underpin a two-by-one genetic model (Figure 1A) that reflects current understanding of CI genetics and embraces various functional models (Figure 1B). A recent article by Beckmann et al. provides interesting ideas about the mechanism and evolutionary history of the CI genes. Therein, they claim that it is 'clearer than ever that the CI induction and rescue stem from a toxin–antidote (TA) system', and that disputes regarding the operon status of the cif genes are semantic. They also propose a new nomenclature to describe the genes. It is important to test hypotheses and develop nomenclature carefully in the context of current data because misconceptions can sometimes become a narrative for those unfamiliar with the evidence. Here, we present and evaluate three points of criticism of the arguments related to the TA model, the operon hypothesis, and the proposed gene nomenclature. We recommend caution and nuance in interpreting current data (and lack thereof). As we will frequently note, more research will be necessary before a functional narrative should be prescribed for CI.