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Cytokinin Biosynthesis Promotes Cortical Cell Responses during Nodule Development. | LitMetric

Cytokinin Biosynthesis Promotes Cortical Cell Responses during Nodule Development.

Plant Physiol

Centre for Carbohydrate Recognition and Signaling, Department of Molecular Biology and Genetics, Aarhus University, Aarhus C 8000, Denmark

Published: September 2017

AI Article Synopsis

Article Abstract

Legume mutants have shown the requirement for receptor-mediated cytokinin signaling in symbiotic nodule organogenesis. While the receptors are central regulators, cytokinin also is accumulated during early phases of symbiotic interaction, but the pathways involved have not yet been fully resolved. To identify the source, timing, and effect of this accumulation, we followed transcript levels of the cytokinin biosynthetic pathway genes in a sliding developmental zone of roots. and were identified as the major contributors to the first cytokinin burst. The genetic dependence and Nod factor responsiveness of these genes confirm that cytokinin biosynthesis is a key target of the common symbiosis pathway. The accumulation of and transcripts occurs independent of the receptor during nodulation. Together with the rapid repression of both genes by cytokinin, this indicates that and contribute to, rather than respond to, the initial cytokinin buildup. Analysis of the cytokinin response using the synthetic cytokinin sensor, , showed that this response occurs in cortical cells before spreading to the epidermis in While mutant analysis identified redundancy in several biosynthesis families, we found that mutation of limits nodule numbers. Overexpression of or alone was insufficient to produce the robust formation of spontaneous nodules. In contrast, overexpressing a complete cytokinin biosynthesis pathway leads to large, often fused spontaneous nodules. These results show the importance of cytokinin biosynthesis in initiating and balancing the requirement for cortical cell activation without uncontrolled cell proliferation.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5580777PMC
http://dx.doi.org/10.1104/pp.17.00832DOI Listing

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