Plant Physiology Preview
Published on June 22, 2007; 10.1104/pp.107.100495
Received April 1, 2007
Accepted June 15, 2007
Medicago LYK3, an Entry Receptor in Rhizobial Nod Factor Signaling
Patrick Smit , Erik Limpens , Rene Geurts , Elena Fedorova , Elena Dolgikh , Clare Gough , and Ton Bisseling *
Laboratory of Molecular Biology, Graduate School of Experimental Plant Sciences, Wageningen University, Wageningen 6703 HA, Netherlands; Laboratoire des Interactions Plantes-Microorganismes INRA-CNRS, BP27, 31326 Castanet-Tolosan Cedex, France
* Corresponding author; email: ton.bisseling{at}wur.nl.
Rhizobia secrete Nod factors that set in motion the formation of nitrogen fixing root nodules on legume host plants. Nod factors induce several cellular responses in root hairs cells within minutes, but are also essential for the formation of infection threads, by which rhizobia enter the root. Based on studies using bacterial mutants a two-receptor model was proposed, a signaling receptor inducing early responses with low requirements towards Nod factor structure, and an entry receptor that controls infection with more stringent demands. Recently, putative Nod factor receptors were shown to be LysM domain receptor kinases. However, mutants in these receptors, in both Lotus japonicus (nfr1 and nfr5) and Medicago truncatula (nfp), do not support the two-receptor model as they lack all Nod factor-induced responses. LYK3, the putative M. truncatula ortholog of NFR1, has only been studied by RNAi showing a role in infection thread formation. M. truncatula hcl mutants are unable to form curled root hairs, a step preceding infection thread formation. We identified the weak hcl-4 allele that is blocked during infection thread growth. We show that HCL encodes LYK3 and thus that this receptor, besides infection, also controls root hair curling. By using rhizobial mutants we also show that HCL controls infection thread formation in a Nod factor structure dependent manner. Therefore LYK3 functions as the proposed entry receptor, specifically controlling infection. Finally we show that NIN, a Nod factor-induced putative transcription factor, acts upstream of LYK3 that in turn regulates a subset of Nod factor induced genes.
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