The mutant developed small white bumps in response to Sinorhizobium meliloti and showed a 4-fold reduction in the number of infections, all of which arrested in the
root epidermis. Nodule primordia initiated normally but failed to mature. Transcriptional markers for early Nod
factor responses (RIP1 and ENOD40) are induced in the mutant, as is another early nodulin, ENOD20, a gene expressed during the differentiation of nodule primordia. By contrast, other markers correlated with primordium differentiation (CCS52A), infection progression (MtN6), or nodule morphogenesis (ENOD2 and ENOD8) show reduced or no induction in homozygous lin individuals.
Single gene targeted?
yes
Extra Information
C88 line was backcrossed to wild type (A17) several rounds to remove background mutations not related to the phenotype. The phenotypic analyses of the mutant suggest that LIN functions downstream of initial events in Nod factor signal transduction, but is required for both infection persistence and nodule differentiation.
Mutagenesis Method
EMS
Mutant Class
Nod-
Allelism
not allelic to dmi1 or pdl
The earliest development stage known to be affected