Modification of tomato growth by expression of truncated ERECTA protein from Arabidopsis thaliana

Hector Villagarcia, Anne Claire Morin, Elena D. Shpak, Mariya V. Khodakovskaya

Resultado de la investigación: Contribución a una revistaArtículo (Contribución a Revista)revisión exhaustiva

32 Citas (Scopus)

Resumen

ERECTA family genes encode leucine-rich repeat receptor-like kinases that control multiple aspects of plant development such as elongation of aboveground organs, leaf initiation, development of flowers, and epidermis differentiation. These receptors have also been implicated in responses to biotic and abiotic stress, probably as a consequence of their involvement in regulation of plant architecture. Here, ERECTA signalling in tomatoes (Solanum lycopersicum) was manipulated by expressing truncated ERECTA protein (AtΔKinase) from Arabidopsis using two different promoters. In Arabidopsis, this protein functions in a dominant-negative manner, disrupting signalling of the whole ERECTA gene family. Expression of AtΔKinase under a constitutive 35S promoter dramatically reduced vegetative growth and led to the formation of fruits with a reduced seed set. Similarly, expression of AtΔKinase under its own promoter resulted in transgenic tomato plants with diminished growth, a reduced number of leaves, changed flowering time, and slightly increased stomata density. The transgenic plants also exhibited increased tolerance to water deficit stress, at least partially due to their diminished surface area. These phenotypes of the transgenic plants were the result of ERECTA signalling disruption at the protein level, as the expression of two endogenous tomato ERECTA family genes was not suppressed. These results demonstrate the significance of ERECTA family genes for development and stress responses in tomato and suggest that truncated ERECTA can be used to manipulate the growth of crop species. .

Idioma originalInglés
Páginas (desde-hasta)6493-6504
Número de páginas12
PublicaciónJournal of Experimental Botany
Volumen63
N.º18
DOI
EstadoPublicada - 1 nov 2012
Publicado de forma externa

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