Enhanced root exudation induces microbial feedbacks to N cycling in a pine forest under long-term CO2 fumigation.

Published

Journal Article

The degree to which rising atmospheric CO(2) will be offset by carbon (C) sequestration in forests depends in part on the capacity of trees and soil microbes to make physiological adjustments that can alleviate resource limitation. Here, we show for the first time that mature trees exposed to CO(2) enrichment increase the release of soluble C from roots to soil, and that such increases are coupled to the accelerated turnover of nitrogen (N) pools in the rhizosphere. Over the course of 3 years, we measured in situ rates of root exudation from 420 intact loblolly pine (Pinus taeda L.) roots. Trees fumigated with elevated CO(2) (200 p.p.m.v. over background) increased exudation rates (μg C cm(-1) root h(-1) ) by 55% during the primary growing season, leading to a 50% annual increase in dissolved organic inputs to fumigated forest soils. These increases in root-derived C were positively correlated with microbial release of extracellular enzymes involved in breakdown of organic N (R(2) = 0.66; P = 0.006) in the rhizosphere, indicating that exudation stimulated microbial activity and accelerated the rate of soil organic matter (SOM) turnover. In support of this conclusion, trees exposed to both elevated CO(2) and N fertilization did not increase exudation rates and had reduced enzyme activities in the rhizosphere. Collectively, our results provide field-based empirical support suggesting that sustained growth responses of forests to elevated CO(2) in low fertility soils are maintained by enhanced rates of microbial activity and N cycling fuelled by inputs of root-derived C. To the extent that increases in exudation also stimulate SOM decomposition, such changes may prevent soil C accumulation in forest ecosystems.

Full Text

Duke Authors

Cited Authors

  • Phillips, RP; Finzi, AC; Bernhardt, ES

Published Date

  • February 2011

Published In

Volume / Issue

  • 14 / 2

Start / End Page

  • 187 - 194

PubMed ID

  • 21176050

Pubmed Central ID

  • 21176050

Electronic International Standard Serial Number (EISSN)

  • 1461-0248

International Standard Serial Number (ISSN)

  • 1461-023X

Digital Object Identifier (DOI)

  • 10.1111/j.1461-0248.2010.01570.x

Language

  • eng