Abstract
AtLSD1, a negative regulator of programmed cell death (PCD) in Arabidopsis, is a retention protein that inhibits nuclear import of transcription factors (TFs: AtbZIP10, IAA8, CBF-C) by its direct interaction via "GxP" motif. The function of AtLSD1 as a negative regulator of PCD supposed to be derived from that as a retention protein, whereas AtLOL1, AtLSD1 homolog, is known as a positive regulator of PCD. In vivo experiments demonstrated AtLOL1 interacts with same TFs via "GxP" motif as AtLSD1. "GxP" mutation on these TFs, which are localized both in nucleus and cytosol, compromised their cytosol localization. These results suggested that interaction between AtLSD1/AtLOL1 and TFs via "GxP" motif is essential for inhibition of their nuclear import. Since overexpression of AtLSD1ΔC, which lacks C-terminal region of AtLSD1 caused LOL1-like PCD phenotype, this region seems to be involved in antagonistic function of AtLSD1 and AtLOL1 on PCD induction.
