Functional traits explain the weakening of biotic resistance to plant invasion under karst soil phosphorus heterogeneity
摘要
The biotic resistance hypothesis posits that species-rich communities are more resistant to invasion, yet its applicability in highly fragmented karst systems remains unclear. Soil nutrient heterogeneity may facilitate invasion via clonal integration, but how karst soil phosphorus (P) heterogeneity influences the mechanisms by which resident diversity resists invasion is unknown.
MethodsWe constructed experimental invasion systems using the globally invasive Ageratina adenophora and 14 resident communities spanning four diversity levels under homogeneous and heterogeneous P conditions. Functional dispersion (FDis) and community-weighted mean traits (CWM) were quantified, and CWM.PC1 was calculated. These metrics were used as latent variables in structural equation modeling (SEM) to identify the mechanisms underlying invasion resistance.
ResultsResident diversity consistently suppressed invasion across P treatments. However, P heterogeneity weakened resistance and altered mechanisms: under low heterogeneity, niche complementarity (higher FDis) primarily drove resistance; at higher heterogeneity, selection mediated by resource-acquisition traits (higher CWM.PC1) became more dominant. SEM revealed that diversity suppressed invasion both directly and indirectly via effects on resident biomass and community structure (FDis and CWM.PC1). Although P heterogeneity indirectly suppressed invasion by enhancing resident biomass and CWM.PC1, its direct positive effect on the invader outweighed this, ultimately reducing resistance.
ConclusionsThis study provides the first empirical test of biotic resistance in karst systems under P heterogeneity, showing that both complementarity and selection contribute to invasion resistance, with their relative importance dependent on nutrient heterogeneity. Maintaining resident diversity is an effective strategy for invasion control, but management should account for environment-dependent shifts in resistance mechanisms.