TY - JOUR
T1 - The BRI1-Associated Kinase 1, BAK1, Has a Brassinolide-Independent Role in Plant Cell-Death Control
AU - Kemmerling, Birgit
AU - Schwedt, Anne
AU - Rodriguez, Patricia
AU - Mazzotta, Sara
AU - Frank, Markus
AU - Qamar, Synan Abu
AU - Mengiste, Tesfaye
AU - Betsuyaku, Shigeyuki
AU - Parker, Jane E.
AU - Müssig, Carsten
AU - Thomma, Bart P.H.J.
AU - Albrecht, Catherine
AU - de Vries, Sacco C.
AU - Hirt, Heribert
AU - Nürnberger, Thorsten
N1 - Funding Information:
We thank K. Schumacher, J. Chory, T. Nakagawa, A. Gust, and F. Tax for materials; V. Lipka and F. Tax for comments; and M. Tör for sharing data. We acknowledge the Salk Institute, Nottingham Arabidopsis Stock Center (NASC), and American Biological Resource Center (ABRC) collections for mutant seeds and the AtGenExpress Initiative for sharing data sets. This work was supported by the Deutsche Forschungsgemeinschaft (Arabidopsis Functional Genomics Network [AFGN], SFB446) (T.N.), Deutscher Akademischer Austauschdienst (P.R.), the Max-Planck-Society DFG SFB 635 (J.E.P.), and The Japan Society for the Promotion of Young Scientists (S.B.).
PY - 2007/7/3
Y1 - 2007/7/3
N2 - Programmed cell death (PCD) is a common host response to microbial infection [1-3]. In plants, PCD is associated with immunity to biotrophic pathogens, but it can also promote disease upon infection by necrotrophic pathogens [4]. Therefore, plant cell-suicide programs must be strictly controlled. Here we demonstrate that the Arabidopsis thaliana Brassinosteroid Insensitive 1 (BRI1)-associated receptor Kinase 1 (BAK1), which operates as a coreceptor of BRI1 in brassinolide (BL)-dependent plant development, also regulates the containment of microbial infection-induced cell death. BAK1-deficient plants develop spreading necrosis upon infection. This is accompanied by production of reactive oxygen intermediates and results in enhanced susceptibility to necrotrophic fungal pathogens. The exogenous application of BL rescues growth defects of bak1 mutants but fails to restore immunity to fungal infection. Moreover, BL-insensitive and -deficient mutants do not exhibit spreading necrosis or enhanced susceptibility to fungal infections. Together, these findings suggest that plant steroid-hormone signaling is dispensable for the containment of infection-induced PCD. We propose a novel, BL-independent function of BAK1 in plant cell-death control that is distinct from its BL-dependent role in plant development.
AB - Programmed cell death (PCD) is a common host response to microbial infection [1-3]. In plants, PCD is associated with immunity to biotrophic pathogens, but it can also promote disease upon infection by necrotrophic pathogens [4]. Therefore, plant cell-suicide programs must be strictly controlled. Here we demonstrate that the Arabidopsis thaliana Brassinosteroid Insensitive 1 (BRI1)-associated receptor Kinase 1 (BAK1), which operates as a coreceptor of BRI1 in brassinolide (BL)-dependent plant development, also regulates the containment of microbial infection-induced cell death. BAK1-deficient plants develop spreading necrosis upon infection. This is accompanied by production of reactive oxygen intermediates and results in enhanced susceptibility to necrotrophic fungal pathogens. The exogenous application of BL rescues growth defects of bak1 mutants but fails to restore immunity to fungal infection. Moreover, BL-insensitive and -deficient mutants do not exhibit spreading necrosis or enhanced susceptibility to fungal infections. Together, these findings suggest that plant steroid-hormone signaling is dispensable for the containment of infection-induced PCD. We propose a novel, BL-independent function of BAK1 in plant cell-death control that is distinct from its BL-dependent role in plant development.
KW - CELLCYCLE
UR - http://www.scopus.com/inward/record.url?scp=34250803478&partnerID=8YFLogxK
U2 - 10.1016/j.cub.2007.05.046
DO - 10.1016/j.cub.2007.05.046
M3 - Article
C2 - 17583510
AN - SCOPUS:34250803478
SN - 0960-9822
VL - 17
SP - 1116
EP - 1122
JO - Current Biology
JF - Current Biology
IS - 13
ER -