Regulation of NB-LRR-type UNI and its related signaling pathway: signaling crosstalk and methodology for quick identification of related factors.

Activation of NB-LRR-related UNI proteins by uni-1D mutation, a gain-of-function mutation of the UNI gene, induces some pathogenesis-related responses and also affects morphology through modulation of meristem activities. In a recent study we reported that the uni-1D phenotypes require cooperative action of ERECTA (ER) receptor kinase family members in UNI-expressing cells, suggesting that an intracellular signaling crosstalk between ER-family-dependent and UNI-triggered signaling pathways plays a significant role in the phenotypes. Further we recently succeeded in the establishment of a methodology for rapid identification of factors involved in the UNI function. EMS-induced causal mutations that suppress the uni-1D phenotypes could be identified using whole-genome-sequencing technologies with much less labor compared with the conventional map-based cloning method that is generally time-consuming and labor-intensive. Thus it would be now possible to intensively identify factors that play significant roles in regulation of UNI proteins and/or UNI-related signaling pathways.