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Published on July 30, 2008; 10.1104/pp.108.123422


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Received May 23, 2008
Accepted July 16, 2008

Roles for the regulation of respiration and the oxygen diffusion barrier in soybean in the protection of symbiotic nitrogen fixation from chilling -induced inhibition and shoots from premature senescence

Philippus D.R. van Heerden , Guy Kiddle , Till K. Pellny , Phatlane W. Mokwala , Anine Jordaan , Abram J. Strauss , Misha de Beer , Urte Schluter , Karl J. Kunert , and Christine H. Foyer *

Plant Sciences Department, Rothamsted Research, Harpenden, Herts AL5 2JQ, United Kingdom; School of Environmental Sciences and Development: Section Botany, North-West University, Potchefstroom 2520, South Africa; Department of Biodiversity, University of Limpopo, Sovenga 0727 South Africa; Forestry and Agricultural Biotechnology Institute (FABI), University of Pretoria, Pretoria 0002 South Africa; School of Agriculture, Food and Rural Development, The University of Newcastle upon Tyne, Newcastle upon Tyne, NE1 7RU, UK

* Corresponding author; email: christine.foyer{at}ncl.ac.uk.

Symbiotic nitrogen fixation (SNF) is sensitive to dark chilling (7-15°C)–induced inhibition in soybean. To characterize the mechanisms that cause the stress-induced loss of nodule function we examined nodule structure, carbon/nitrogen interactions and respiration in two soybean genotypes that differ in chilling-sensitivity: PAN809 (PAN), which is chilling-sensitive and Highveld Top (HT), which is more chilling-resistant. Nodule numbers were unaffected by dark chilling, as was the abundance of the nitrogenase and leghemoglobin proteins. However, dark chilling decreased nodule respiration rates, nitrogenase activity and NifH and NifK mRNAs and increased nodule starch, sucrose and glucose in both genotypes. Ureide and fructose contents decreased only in PAN nodules. While the chilling-induced decreases in nodule respiration persisted in PAN even after return to optimal temperatures, respiration started to recover in HT by the end of the chilling period. The area of the intercellular spaces in the nodule cortex and infected zone was greatly decreased in HT after 3 nights of chilling, an acclimatory response that were absent from PAN. These data show that HT nodules are able to regulate both respiration and the area of the intercellular spaces during chilling and in this way control the oxygen diffusion barrier, which is a key component of the nodule stress response. We conclude that chilling-induced loss of SNF in PAN is caused by the inhibition of respiration coupled to the failure to regulate the oxygen diffusion barrier effectively. The resultant limitations on nitrogen availability contribute to the greater chilling-induced inhibition of photosynthesis in PAN than HT.




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