Abstract
Nicotinamide adenine dinucleotide (NAD) plays important roles in regulating cell homeostasis and responses to various stressful environments. In Arabidopsis, genes involved in the NAD biosynthetic pathway have been fully determined. Out of these, a gene encoding nicotinate/nicotinamide mononucleotide adenyltransferase (NMNAT), AtNMNAT, is critical for the NAD biosynthesis because the NMNAT acts in de novo and salvage pathway. Previously, we reported an ABA-induced posttranscriptional activation of NMNAT in stomatal guard cells. In this study, we found that GST-NMNAT forms homomeric complex with enzymatic activity in vitro. Interestingly, expression of truncated NMNAT with no enzymatic activity suppressed endogenous NMNAT activity in vivo, meaning that truncated form of NMNAT acts as a dominant negative. Interestingly, the formation of complex was reppressed in an ABA-insensitive mutant where NAD decrease did not occur. These results suggest that the level of cellular NAD is maintained by regulating the biosynthetic activity through the modulation of NMNAT complex.
