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Nodulation factor receptor kinase 1α controls nodule organ number in soybean ( Glycine max L. Merr)
Author(s) -
Indrasumunar Arief,
Searle Iain,
Lin MengHan,
Kereszt Attila,
Men Artem,
Carroll Bernard J.,
Gresshoff Peter M.
Publication year - 2011
Publication title -
the plant journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.058
H-Index - 269
eISSN - 1365-313X
pISSN - 0960-7412
DOI - 10.1111/j.1365-313x.2010.04398.x
Subject(s) - biology , mutant , complementation , bradyrhizobium japonicum , gene , transgene , glycine , bradyrhizobium , lotus japonicus , root nodule , frameshift mutation , genetics , allele , microbiology and biotechnology , mutation , rhizobiaceae , nitrogen fixation , amino acid , symbiosis , rhizobium , bacteria
Summary Two allelic non‐nodulating mutants, nod49 and rj1 , were characterized using map‐based cloning and candidate gene approaches, and genetic complementation. From our results we propose two highly related lipo‐oligochitin LysM‐type receptor kinase genes ( GmNFR1α and GmNFR1β ) as putative Nod factor receptor components in soybean. Both mutants contained frameshift mutations in GmNFR1α that would yield protein truncations. Both mutants contained a seemingly functional GmNFR1β homeologue, characterized by a 374‐bp deletion in intron 6 and 20–100 times lower transcript levels than GmNFR1α , yet both mutants were unable to form nodules. Mutations in GmNFR1β within other genotypes had no defects in nodulation, showing that GmNFR1β was redundant. Transgenic overexpression of GmNFR1α , but not of GmNFR1β , increased nodule number per plant, plant nitrogen content and the ability to form nodules with restrictive, ultra‐low Bradyrhizobium japonicum titres in transgenic roots of both nod49 and rj1 . GmNFR1α overexpressing roots also formed nodules in nodulation‐restrictive acid soil (pH 4.7). Our results show that: (i) NFR1α expression controls nodule number in soybean, and (ii) acid soil tolerance for nodulation and suppression of nodulation deficiency at low titre can be achieved by overexpression of GmNFR1α .