Prof. Zhonglin Mou
Microbiology and Cell Science, University of Florida
Friday, October 24, 2014 - 2:00pm
Ramsay Wright Building, Room 432
Emerging evidence from research in mammalian cells has indicated that cellular NAD(P) can be actively or passively released into the extracellular compartment (ECC), where NAD(P) is processed or perceived by ectoenzymes or cell-surface receptors/channels, leading to transmembrane signaling. Surprisingly, no homologous proteins of mammalian ectoenzymes have been identified in plants, which calls into question whether extracellular NAD(P) [eNAD(P)] and eNAD(P)-activated signaling pathways exist in plants. We found that exogenous application of NAD(P) induces immune responses without changing intracellular NAD(P) homeostasis in Arabidopsis, suggesting that NAD(P) may function in the ECC of plant cells. Moreover, during pathogen infection, cellular NAD(P) is released into the ECC and the amount of NAD(P) released is sufficient for activating immune responses in Arabidopsis. These data suggest that eNAD(P) may act as an endogenous elicitor in plant immune response. Supporting this hypothesis, the well-characterized human NAD(P)-metabolizing ectoenzyme CD38, when expressed in Arabidopsis, suppresses eNAD+-induced defense gene expression and disease resistance, indicating that the mechanisms used by plants to process or perceive eNAD(P) for immune response activation may not be the same as those in mammalian cells. Presently eNAD(P)-activated signaling networks in plants remain undefined and how eNAD(P) is processed or perceived by plant cells is unknown. We are addressing these questions through microarray and genetic experiments. Results of these experiments and possible plant cell-surface targets/receptors of eNAD(P) will be discussed.
Prof. Keiko Yoshioka
Dept of Cell and Systems Biology