Priming of carbon and nitrogen mineralization in forest soils
Author
Summary, in English
Decomposition of soil organic matter (SOM) contributes significantly to the global carbon (C) cycle and climate feedbacks. SOM decomposition depends on soil microbial activities, and these activities are driven by the availability of C and other nutrients. Plant root exudates are known to alter decomposition of SOM, a phenomenon referred to as rhizosphere priming effects (RPE). In order to predict the effect of environmental changes such as elevated CO2 and increased N deposition on microbial SOM decomposition and release of CO2 to the atmosphere, we need a better understanding of the factors that regulate RPE.
In this thesis, I present my results from priming experiments with and without plants. I studied the effect of root exudates on SOM decomposition by adding glucose to soil to simulate root exudation. I also performed experiments with living plants. The aim was to investigate how variations in C and N availability influence priming. I further aimed to determine how elevated CO2, N fertilization, and light intensity influence root exudation rates and priming. I also tested how priming influence gross N mineralization and protein depolymerization, and if this could be linked to the abundance of different microbial functional groups and extracellular enzyme activity.
I found that the soil C:N ratio is a poor predictor of priming. Instead, my findings suggest that the C:N imbalance (soil C:N divided by microbial biomass C:N) could better predict priming. My findings suggest that C:N imbalances could induce priming by increasing the abundance of microbes able to decompose complex substrates such as lignin. My results further suggest that priming is a result of enhanced activity of extracellular oxidative enzymes, rather than a change in the concentration of enzymes. I also found that in addition to increasing N cycling rates, soil microbes could meet their increased N demand caused by C input through using the available N more efficiently. This suggests that plant C input might aggravate N limitation by promoting microbial N sequestration.
My findings highlight that elevated CO2 and N deposition enhance plant C uptake, but they also increase the microbial respiration of SOM to an even greater extent. These findings suggest that in order to evaluate if elevated CO2 and N deposition increases terrestrial C sequestration, changes in the microbial decomposition of SOM also needs to be accounted for. Finally, my results demonstrated that physiological traits of different plant species, e.g. response to altered light intensity, also have important effects on RPE.
In summary, my findings suggest that priming is of major importance not only for C cycling in forest soils, but also for N cycling. Stoichiometric imbalances in C and N, plant and microbial nutrient demands, and the microbial response to nutrient deficiency, are important factors regulating RPE. I also conclude that priming a result of stimulated activity of extracellular oxidative enzymes, rather than of increased concentration of such enzymes.
In this thesis, I present my results from priming experiments with and without plants. I studied the effect of root exudates on SOM decomposition by adding glucose to soil to simulate root exudation. I also performed experiments with living plants. The aim was to investigate how variations in C and N availability influence priming. I further aimed to determine how elevated CO2, N fertilization, and light intensity influence root exudation rates and priming. I also tested how priming influence gross N mineralization and protein depolymerization, and if this could be linked to the abundance of different microbial functional groups and extracellular enzyme activity.
I found that the soil C:N ratio is a poor predictor of priming. Instead, my findings suggest that the C:N imbalance (soil C:N divided by microbial biomass C:N) could better predict priming. My findings suggest that C:N imbalances could induce priming by increasing the abundance of microbes able to decompose complex substrates such as lignin. My results further suggest that priming is a result of enhanced activity of extracellular oxidative enzymes, rather than a change in the concentration of enzymes. I also found that in addition to increasing N cycling rates, soil microbes could meet their increased N demand caused by C input through using the available N more efficiently. This suggests that plant C input might aggravate N limitation by promoting microbial N sequestration.
My findings highlight that elevated CO2 and N deposition enhance plant C uptake, but they also increase the microbial respiration of SOM to an even greater extent. These findings suggest that in order to evaluate if elevated CO2 and N deposition increases terrestrial C sequestration, changes in the microbial decomposition of SOM also needs to be accounted for. Finally, my results demonstrated that physiological traits of different plant species, e.g. response to altered light intensity, also have important effects on RPE.
In summary, my findings suggest that priming is of major importance not only for C cycling in forest soils, but also for N cycling. Stoichiometric imbalances in C and N, plant and microbial nutrient demands, and the microbial response to nutrient deficiency, are important factors regulating RPE. I also conclude that priming a result of stimulated activity of extracellular oxidative enzymes, rather than of increased concentration of such enzymes.
Publishing year
2019-01
Language
English
Volume
1
Full text
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Document type
Dissertation
Publisher
Biologiska institutionen, Lunds universitet
Topic
- Ecology
Keywords
- Soil organic matter
- C:N imbalance
- root exudates
- priming
- Extracellular enzymes
- Soil organic matter
- C:N imbalance
- root exudates
- priming
- Extracellular enzymes
Status
Published
Supervisor
ISBN/ISSN/Other
- ISBN: 978-91-7753-947-6
- ISBN: 978-91-7753-946-9
Defence date
15 February 2019
Defence time
10:00
Defence place
Blue Hall, The Ecology Building, Sölvegatan 37, Lund
Opponent
- Eric Paterson (Dr.)