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Background: Environmental parental effects can have important ecological and evolutionary consequences, yet little is known about genetic variation among populations in the plastic responses of offspring phenotypes to parental environmental conditions. This type of variation may lead to rapid phenotypic divergence among populations and facilitate speciation. With respect to density- dependent phenotypic plasticity, locust species ( Orthoptera: family Acrididae), exhibit spectacular developmental and behavioural shifts in response to population density, called phase change. Given the significance of phase change in locust outbreaks and control, its triggering processes have been widely investigated. Whereas crowding within the lifetime of both offspring and parents has emerged as a primary causal factor of phase change, less is known about intraspecific genetic variation in the expression of phase change, and in particular in response to the parental environment. We conducted a laboratory experiment that explicitly controlled for the environmental effects of parental rearing density. This design enabled us to compare the parental effects on offspring expression of phase- related traits between two naturally- occurring, genetically distinct populations of Locusta migratoria that differed in their historical patterns of high population density outbreak events.

Results: We found that locusts from a historically outbreaking population of L. migratoria expressed parentally- inherited density- dependent phase changes to a greater degree than those from a historically non- outbreaking population.

Conclusion: Because locusts from both populations were raised in a common environment during our experiment, a genetically- based process must be responsible for the observed variation in the propensity to express phase change. This result emphasizes the importance of genetic factors in the expression of phase traits and calls for further investigations on density- dependent parental effects in locust phase change. More population samples with different outbreak histories need to be analyzed to demonstrate that differences in propensity to gregarise evolve because of different outbreak histories.