Lotus japonicus Cytokinin Receptors Work Partially Redundantly to Mediate Nodule Formation
Previous analysis of the Lotus histidine kinase1 (Lhk1) cytokinin receptor gene has shown that it is required and also sufficient for nodule formation in Lotus japonicus. The L. japonicus mutant carrying the loss-of-function lhk1-1 allele is hyperinfected by its symbiotic partner, Mesorhizobium loti...
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Published in | The Plant cell Vol. 26; no. 2; pp. 678 - 694 |
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Main Authors | , , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
England
American Society of Plant Biologists
01.02.2014
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Subjects | |
Online Access | Get full text |
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Summary: | Previous analysis of the Lotus histidine kinase1 (Lhk1) cytokinin receptor gene has shown that it is required and also sufficient for nodule formation in Lotus japonicus. The L. japonicus mutant carrying the loss-of-function lhk1-1 allele is hyperinfected by its symbiotic partner, Mesorhizobium loti, in the initial absence of nodule organogénesis. At a later time point following bacterial infection, lhk1-1 develops a limited number of nodules, suggesting the presence of an Lhk1-independent mechanism. We have tested a hypothesis that other cytokinin receptors function in at least a partially redundant manner with LHK1 to mediate nodule organogenesis in L. japonicus. We show here that L. japonicus contains a small family of four cytokinin receptor genes, which all respond to M. Ioti infection. We show that within the root cortex, LHK1 performs an essential role but also works partially redundantly with LHK1A and LHK3 to mediate cell divisions for nodule primordium formation. The LHK1 receptor is also presumed to partake in mediating a feedback mechanism that negatively regulates bacterial infections at the root epidermis. Interestingly, the Arabidopsis thaliana AHK4 receptor gene can functionally replace Lhk1 in mediating nodule organogenesis, indicating that the ability to perform this developmental process is not determined by unique, legume-specific properties of LHK1. |
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Bibliography: | Current address: Graduate School of Life Sciences, Tohoku University, 2-1-1 Katahira, Sendai 980-8577, Japan. These authors contributed equally to this work. Current address: Biotechnology Institute, University of Minnesota, Saint Paul, MN 55108. The author responsible for distribution of materials integral to the findings presented in the article in accordance with the policy described in the Instructions for Authors (www.plantcell.org) is: Krzysztof Szczyglowski (krzysztof.szczyglowski@agr.gc.ca). www.plantcell.org/cgi/doi/10.1105/tpc.113.119362 |
ISSN: | 1040-4651 1532-298X |
DOI: | 10.1105/tpc.113.119362 |