IN INOCULANTS Nodulaid - 17th International Nitrogen Fixation ...

17 th International Congress on Nitrogen Fixation
Fremantle, Western Australia
27 November – 1 December 2011
Session Details: Tuesday 29 November 2011
Concurrent Session 8 – Plant Symbiotic Genes
1600 – 1720
Authors: Nijat Imin 1 , Isabel Saur 1 , Nadiatul Radzman 1 , Marie Oakes 1 , Michael A Djordjevic 1
1 Plant Science Division and A. R. C. Centre of Excellence for Integrative Legume
Research , Research School of Biology, Canberra, 0200, Australia.
Presentation Title: Nodule specific CLE peptides mediate crosstalk between local nodule development and
systemic autoregulation of nodulation pathways
Presentation Time: 1640 – 1700
Root nodulation is controlled by the local Nod Factor and cytokinin-dependent pathways and systemically by the
autoregulation of nodulation (AON) pathway (1). The AON pathway controls nodule number by suppressing nodulation
competency in yet-to-be-infected roots via the shoot-expressing SUNN receptor kinase (1-3).
Recently, MtCLE12 and MtCLE13, which show nodule-specific expression and encode CLE (CLAVATA3/ESR) peptide
ligands, have been shown to regulate AON (3). The ectopic expression of MtCLE12 or MtCLE13 (but not MtCLE26 which
does not have nodule specific expression) abolishes nodulation in wild type roots but not in the super nodulating null mutant
sunn-4. This suggests that root MtCLE12 or 13 over-expression triggers constitutive AON which suppresses nodulation
competency in a SUNN-dependent manner. Using qRT-PCR, we show that three local nodulation pathway genes: NODULE
INCEPTION (NIN, a common regulator of the Nod Factor and cytokinin pathways), MtEFD (ethylene response factor and
negative regulator of nodule differentiation) and MtRR8 (a type-A response regulator involved in negatively regulating
cytokinin signaling) are each regulated specifically by MtCLE12 in a SUNN-dependent manner. This suggests that MtCLE12
expression in the first formed nodules influences shoot SUNN to produce the AON signal that travels to the yet-to-be
infected roots to up regulate MtEFD and MtRR8 to reduce nodulation competency by down regulating NIN. This would
suppress local Nod Factor and cytokinin signaling at a common point: NIN. This proposed model links for the first time the
pathways for Nod factor signaling, cytokinin perception and AON and provides a means for the plant to exert a mechanism
to regulate nodule numbers in tune with its physiological status.
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