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Plant and Cell Physiology, 2003, Vol. 44, No. 3 255-261
© 2003 Oxford University Press

Deletion of a Chaperonin 60ß Gene Leads to Cell Death in the Arabidopsis lesion initiation 1 Mutant

Atsushi Ishikawa1,3, Hideaki Tanaka1, Masato Nakai2 and Tadashi Asahi1

1 Department of Bioscience, Fukui Prefectural University, Fukui, 910-1195 Japan
2 Institute for Protein Research, Osaka University, 3-2 Yamadaoka, Suita, Osaka, 565-0871 Japan

Lesion mimic mutants develop spontaneous cell death without pathogen attack. Some of the genes defined by these mutations may function as regulators of cell death, whereas others may perturb cellular metabolism in a way that leads to cell death. To understand the molecular mechanism of cell death in lesion mimic mutants, we isolated a lesion initiation 1 (len1) mutant by a T-DNA tagging method. The len1 mutant develops lesions on its leaves and expresses systemic acquired resistance (SAR). LEN1 was identified to encode a chloroplast chaperonin 60ß (Cpn60ß), a homologue of bacterial GroEL. The recombinant LEN1 had molecular chaperone activity for suppressing protein aggregation in vitro. Moreover, len1 plants develop accelerated cell death to heat shock stress in comparison with wild-type plants. The chlorophyll a/b binding protein (CAB) was present in len1 plants at a lower level than in the wild-type plants. These results indicate that LEN1 functions as a molecular chaperone in chloroplasts and its deletion leads to cell death in Arabidopsis.

3 Corresponding author: E-mail, ishikawa{at}fpu.ac.jp; Fax, +81-776-61-6015.


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