Abstract
Previously, OsNIN8 initiated a sucrose signal for cell division in radicle and seed development in rice. Here, a set of genes was induced in starved sprouts after sucrose treatment, and 14 genes were screened between ZH11 and nin8 as reporters of sucrose signal. Expressions of reporter depended on levels of OsNIN8 in overexpression and RNAi lines. Further, OsNIN8 interacted with OsFKBP12, a regulator of TOR signal for cell division, and OsFKBP12 interacted with OsTOR (OsTORKD). However, interactions of OsFKBP12 with OsNIN8 or OsTORKD were a loose binding depending on the hydrophobicity of OsFKBP12 C-terminus in Y2H. In addition, OsFKBP12 associating with OsNIN8 was endothermic but with OsNIN8m was exothermic. Knockout OsFKBP12 reappeared nin8 phenotypes and the complementation of the knockout with C-termini of OsFKBP12 worsened the phenotypes. Treatment with TOR inhibitors caused short radicle and OsTOR RNAi repeated low seed-setting of the phenotypes. So, OsFKBP12 transduced sucrose signal from OsNIN8 to the TOR pathway.