Abstract

Systemic Epichloe endophytes produce alkaloids that protect their grass hosts against pathogens and herbivores. These alkaloids, together with other endophyte induced changes in litter quality, may decelerate the decomposition of infected grass litter, but so far no study has tested whether the effects on decomposition rate translate into changes in N cycling in infected grasslands. Here we test if the Epichloe uncinata infection of meadow fescue, Schedonorus pratensis decelerates litter decomposition and N release, increases soil C and N accumulation and lowers the availability of mineral N in the soil under infected grass. To analyze grass litter and soil attributes, samples were collected from endophyte infected (E+) and non-infected (E-) field plots, established seven years earlier. At the time of the study, the frequency of E+ plants was 80–90 % and 0–3 % in the E+ and E- plots, respectively. Litter decomposition rate and litter N release were examined using litter mesh bags, placed on field ground. Soil mineral N availability was estimated using ion exchange resin bags that were buried in the soil. Epichloe uncinata infection did not affect meadow fescue litter N%, litter mass loss or litter N release. Neither did soil C and N content and resin NH4 and NO3 contents differ between the E+ and E- grass plots. E+ litter did not decompose faster in E+ than E- plots, i.e. no home-field advantage was observed. We did not find evidence that Epichloe uncinata infection would decelerate N cycling and reduce N mineralization in meadow fescue grasslands. This suggests that the infection may not decrease the benefit of the endophyte-grass symbiosis by reducing soil fertility.

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