Differential Roles of Two Homologous Cyclin-Dependent Kinase Inhibitor Genes in Regulating Cell Cycle and Innate Immunity in Arabidopsis
H. LU (1), S. Hamdoun (2), C. Zhang (1), M. Gill (1), N. Kumar (3), M. Churchman (3), J. Larkin (3), A. Kwon (1) (1) University of Maryland Baltimore County, U.S.A.; (2) University of Maryland Baltimore County, U.S.A.; (3) Louisiana State University, U.S.A.

Precise cell cycle control is critical for plant development and responses to pathogen invasion. Two homologous cyclin-dependent kinase inhibitor (CKI) genes, SIAMESE (SIM) and SIM-RELATED 1 (SMR1), were recently shown to regulate Arabidopsis defense based on phenotypes conferred by a sim smr1 double mutant. However whether these two genes play differential roles in cell cycle and defense control is unknown. In this report, we showed that while acting synergistically to promote endoreplication, SIM and SMR1 play different roles in affecting the ploidy of trichome and leaf cells, respectively. In addition, we found that the smr1-1 mutant but not sim-1 was more susceptible to a virulent Pseudomonas syringae strain and this susceptibility could be rescued by activating salicylic acid (SA)-mediated defense. Consistent with these results, smr1-1 partially suppressed the dwarfism, high SA levels, and cell death phenotypes in acd6-1, a mutant used to gauge the change of defense levels. Thus SMR1 functions partly through SA in defense control. The differential roles of SIM and SMR1 are due to differences in temporal and spatial expression of these two genes in Arabidopsis tissues and in response to P. syringae infection. In addition flow cytometry analysis of plants with altered SA signaling revealed that SA is necessary but not sufficient to change cell cycle progression. We further found that a mutant with three CYCD3 genes disrupted also compromised disease resistance to P. syringae. Together this study reveals differential roles of two homologous CKIs in regulating cell cycle progression and innate immunity in Arabidopsis and provides insights into the importance of cell cycle control during host-pathogen interactions.

Abstract Number: P18-682
Session Type: Poster