Herbivory imposes substantial selection pressure on plants, with the ability to
regrow and maintain reproductive success a challenging but often necessary
response by the plant. Despite the commonality of herbivore-induced damage,
vast variation in tolerance ability exists among plants. Recent studies have
suggested the role of endoreduplication (increasing ploidy within an individual)
and the pentose phosphate pathway (a metabolic pathway that supports both
primary and secondary metabolism) in contributing to the variation in tolerance
ability among genotypes of Arabidopsis thaliana. In this study, we sought to
determine whether variation in apical meristem damage frequency,
endoreduplication, and the sequence of G6PD1, an important gene in the pentose
phosphate pathway, significantly contribute to variation in tolerance and
whether this variation corresponds with the geographic distribution of natural
populations of A. thaliana over a portion of its native range. We specifically compared fruit production of undamaged plants with that of naturally damaged plants in populations of France, Germany, and the Netherlands, and analyzed these plants for ploidy and G6PD1 sequence.
Results/Conclusions
We report that for each of five sampled populations, damaged plants had equal
fitness to undamaged plants overall, counter to the widely-held presumption that
reduced plant fitness is the most common result of herbivore damage. Further,
we discovered a likely loss-of-function G6PD1 allele in two populations, both of
which exhibited non-significant trends toward undercompensation. No significant
differences between undamaged and damaged plants in endopolyploidy were found,
though trends toward slight increases match the results of previous studies for
equally-compensating A. thaliana genotypes. Together, this study provides
evidence that plant tolerance of damage is a common phenomenon in natural
populations, contrary to long-held theory, and contributes to the growing body
of research on the contributions of specific molecular mechanisms to the
tolerance response.