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Modification of plant R ac/ R op GTP ase signalling using bacterial toxin transgenes
Author(s) -
Singh Manoj K.,
Ren Fugang,
Giesemann Torsten,
Bosco Cristina Dal,
Pasternak Taras P.,
Blein Thomas,
Ruperti Benedetto,
Schmidt Gudula,
Aktories Klaus,
Molendijk Arthur J.,
Palme Klaus
Publication year - 2013
Publication title -
the plant journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.058
H-Index - 269
eISSN - 1365-313X
pISSN - 0960-7412
DOI - 10.1111/tpj.12040
Subject(s) - gtp' , toxin , transgene , biology , microbiology and biotechnology , chemistry , biochemistry , enzyme , gene
Summary Bacterial protein toxins which modify R ho GTP ase are useful for the analysis of R ho signalling in animal cells, but these toxins cannot be taken up by plant cells. We demonstrate in vitro deamidation of A rabidopsis R op4 by E scherichia coli C ytotoxic N ecrotizing F actor 1 ( CNF 1) and glucosylation by C lostridium difficile toxin B . Expression of the catalytic domain of CNF 1 caused modification and activation of co‐expressed A rabidopsis R op4 GTP ase in tobacco leaves, resulting in hypersensitive‐like cell death. By contrast, the catalytic domain of toxin B modified and inactivated co‐expressed constitutively active R op4, blocking the hypersensitive response caused by over‐expression of active R ops. In transgenic A rabidopsis, both CNF 1 and toxin B inhibited R op‐dependent polar morphogenesis of leaf epidermal cells. Toxin B expression also inhibited R op‐dependent morphogenesis of root hairs and trichome branching, and resulted in root meristem enlargement and dwarf growth. Our results show that CNF 1 and toxin B transgenes are effective tools in R op GTP ase signalling studies.