| Autor: |
Miri, Mandana, Janakirama, Preetam, Huebert, Terry, Ross, Loretta, McDowell, Tim, Orosz, Kathleen, Markmann, Katharina, Szczyglowski, Krzysztof |
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| Zdroj: |
New Phytologist; May2019, Vol. 222 Issue 3, p1523-1537, 15p, 2 Color Photographs, 6 Graphs |
| Abstrakt: |
Summary: During Lotus japonicus–Mesorhizobium loti symbiosis, the LOTUS HISTIDINE KINASE1 (LHK1) cytokinin receptor regulates both the initiation of nodule formation and the scope of root infection. However, the exact spatiotemporal mechanism by which this receptor exerts its symbiotic functions has remained elusive.In this study, we performed cell type‐specific complementation experiments in the hyperinfected lhk1‐1 mutant background, targeting LHK1 to either the root epidermis or the root cortex. We also utilized various genetic backgrounds to characterize expression of several genes regulating symbiotic infection.We show here that expression of LHK1 in the root cortex is required and sufficient to regulate both nodule formation and epidermal infections. The LHK1‐dependent signalling that restricts subsequent infection events is triggered before initial cell divisions for nodule primordium formation. We also demonstrate that AHK4, the Arabidopsis orthologue of LHK1, is able to regulate M. loti infection in L. japonicus, suggesting that an endogenous cytokinin receptor could be sufficient for engineering nitrogen‐fixing root nodule symbiosis in nonlegumes.Our data provide experimental evidence for the existence of an LHK1‐dependent root cortex‐to‐epidermis feedback mechanism regulating rhizobial infection. This root‐localized regulatory module functionally links with the systemic autoregulation of nodulation (AON) to maintain the homeostasis of symbiotic infection. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
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