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Evidence for a Role of the N Terminus and Leucine-Rich Repeat Region of the Mi Gene Product in Regulation of Localized Cell Death
Author(s) -
ChinFeng Hwang,
Amit V. Bhakta,
G. M. Truesdell,
Waclawa M. Pudlo,
Valerie M. Williamson
Publication year - 2000
Publication title -
the plant cell
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.324
H-Index - 341
eISSN - 1532-298X
pISSN - 1040-4651
DOI - 10.1105/tpc.12.8.1319
Subject(s) - nicotiana benthamiana , gene , biology , programmed cell death , amino acid , phenotype , hypersensitive response , peptide sequence , genetics , leucine rich repeat , gene product , microbiology and biotechnology , plant disease resistance , gene expression , apoptosis
The tomato Mi gene confers resistance against root-knot nematodes and potato aphids. Chimeric constructs of the functional gene, Mi-1. 2, with a homolog, Mi-1.1, were produced, and their phenotypes were examined in Agrobacterium rhizogenes-transformed roots. Exchange of the leucine-rich repeat (LRR) region of Mi-1.1 into Mi-1.2 resulted in the loss of ability to confer nematode resistance, as did substitution of a 6-amino acid sequence from the Mi-1.1 LRR into Mi-1.2. Introduction of the Mi-1.2 LRR-encoding region into Mi-1.1 resulted in a lethal phenotype, as did substitution of the fragment encoding the N-terminal 161 amino acids of Mi-1.1 into Mi-1.2. Transient expression of the latter two chimeric constructs in Nicotiana benthamiana leaves produced localized cell death. The cell death caused by the N-terminal exchange was suppressed by coinfiltration with a construct expressing the N-terminal 161 amino acids of Mi-1.2. The phenotypes of these and other constructs indicate that the LRR region of Mi-1.2 has a role in signaling localized cell death and that the N-terminal 161 amino acids have a role in regulating this death.

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