Open AccessCytokinin Induction of Root Nodule Primordia in Lotus japonicus Is Regulated by a Mechanism Operating in the Root Cortex
Author(s) -
Anne B. Heckmann,
Niels Sandal,
Anita S. Bek,
Lene Heegaard Madsen,
Anna Jurkiewicz,
Mette Wibroe Nielsen,
Leïla Tirichine,
Jens Stougaard
Publication year - 2011
Publication title -
molecular plant-microbe interactions
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.565
H-Index - 153
eISSN - 1943-7706
pISSN - 0894-0282
DOI - 10.1094/mpmi-05-11-0142
Subject(s) - lotus japonicus , cytokinin , primordium , lateral root , biology , microbiology and biotechnology , mutant , rhizobia , epidermis (zoology) , nod factor , cortex (anatomy) , root nodule , botany , symbiosis , arabidopsis , gene , genetics , auxin , anatomy , neuroscience , bacteria
Cytokinin plays a central role in the formation of nitrogen-fixing root nodules following inoculation with rhizobia. We show that exogenous cytokinin induces formation of discrete and easily visible nodule primordia in Lotus japonicus roots. The expression of nodulin genes was up-regulated upon cytokinin treatment, suggesting that the genuine nodulation program was indeed activated. This offers a simple approach for dissecting the underlying mechanism. Cytokinin-induced nodule primordia formation was unperturbed in several loss-of-function mutants impaired in epidermal responses to either rhizobial infection, Nod factor application, or both. However, absence of primordia in nsp1, nsp2, and nin mutants showed the requirement for these transcriptional regulators in the cytokinin-mediated activation of the root cortex. Distinguishing the epidermal and cortical responses further, we found that external cytokinin application induced expression of the Nin::GUS reporter gene within the root cortex but not in the root epidermis. Using L. japonicus lhk1-1 and har1 mutants, we demonstrate that discrete activation of root cortical cells by cytokinin depends on the LHK1 cytokinin receptor and is subjected to HAR1-mediated autoregulation.