Caution Does Not Preclude Predictive and Testable Models of Cytoplasmic Incompatibility: A Reply to Shropshire et al.

Scientists often face a dilemma: should they produce explicit, predictive models to explain a body of incomplete data, at the risk of missing some critical aspects, or should they accumulate additional observations, allowing more objective and realistic models to emerge. There is a genuine trade-off between these two positions, which tend to be given different weights by different scientific disciplines, from quantum physics to anthropology. The comments of Shropshire et al. [ 1. Shropshire J.D. et al. Models and nomenclature for cytoplasmic incompatibility: caution over premature conclusions. Trends Genet. 2019; (in press)https://doi.org/10.1016/j.tig.2019.03.004 Scopus (22) Google Scholar ], who we thank for having given attention to our recent Opinion paper [ 2. Beckmann J.F. et al. The toxin–antidote model of cytoplasmic incompatibility: genetics and evolutionary implications. Trends Genet. 2019; 35: 175-185 Abstract Full Text Full Text PDF PubMed Scopus (68) Google Scholar ], illustrate that, in the fields of molecular and evolutionary genetics, there are also different views on where one should stand with respect to this trade-off. Our colleagues argue that caution should prevent us from stating that cytoplasmic incompatibility (CI) induction and rescue most likely stem from a toxin–antidote (TA) system encoded by Wolbachia endosymbionts. We can only agree that caution is always advisable. However, the understanding of CI, with its long theoretical and empirical history, has, in our view, come to a stage where explicit and testable models can and should be formulated.