“…Among them, three lines differing in the genetic basis of hypernodulation were selected, namely mutants of the SYM28, SYM29, and NOD3 genes (Sagan and Duc 1996;Postma et al 1988;Krusell et al 2002). Among diverse mutants of each gene, we first selected the allele displaying the weakest hypernodulating phenotype, i.e., which displayed the least depressed shoot growth compared to the parental line (i.e., P64, P118, and P121 mutants for the SYM28, SYM29, and NOD3 genes, respectively; Bourion et al 2007). In the 2009 experiment, wild type Frisson was grown together with an allelic series of the seven hypernodulating mutants of SYM29 (P118, P87, P90, P89, P91, P93, and P122), each differing in sequence of the sym29 allele (Krusell et al 2002) and varying in hypernodulating intensity, as described in Voisin et al 2013.…”