Main Comments
Our interpretation of the main concern of the PREreview was the strength of the evolutionary conclusions given specific experimental considerations. We fully agree that this is not the perfect experiment but would like to note that this is still the first large scale attempt of this kind of cross-genera host-pathogen interaction using tens of thousands or replicated lesion assessments. We are thinking that our introduction may have contributed to the concern that the evolutionary conclusions are too far by creating an inappropriate dichotomy of this system against strong co-evolutionary systems. We think that we can partly alleviate some of these concerns by further working on the entire manuscript to illustrate that there are a large number of plant-biotic interactions that involve broad spectrum generalists that do not involve the creation of strong-selective pressures on either organism. For example, microbiome work is showing that there are microbes that interact across extensive host ranges. Similarly, there are insects, nematodes, etc that also have extensive host ranges while not imparting dramatic selective pressures. But these organisms still likely create small to moderate extensive pressures that over time would create changes in the hosts. There are extensive arms-race models as noted and these rely on strong, almost winner take all, fitness consequences in the system. Our intent was to develop Botrytis as a model for how generalist interactions dominated by small to moderate fitness consequences may or may not shift across host species looking at both within and between species variation. We feel that by over-emphasizing the lack of fit to the strong fitness arms-race models that we have lost this novelty in the data. For example, we should not have implied this we are working towards a co-evolutionary hypothesis but instead a simple evolutionary hypothesis of how host and pathogen variation may be shaped in these systems. Then future work will have to really dive into potential hypothesis. For example, are the observed interactions due to allele specific interactions across 1000s of genes where the hosts variation is largely shaped by other pathogens and the generalist is simply using an array of flexible responses to occupy opportunistic niches.