Expression of three galactinol synthase isoforms in Coffea arabica L. and accumulation of raffinose and stachyose in response to abiotic stresses.

Autor: dos Santos TB; Instituto Agronômico do Paraná (IAPAR), Laboratório de Biotecnologia Vegetal, Londrina PR, Brazil., Budzinski IG, Marur CJ, Petkowicz CL, Pereira LF, Vieira LG
Jazyk: angličtina
Zdroj: Plant physiology and biochemistry : PPB [Plant Physiol Biochem] 2011 Apr; Vol. 49 (4), pp. 441-8. Date of Electronic Publication: 2011 Feb 01.
DOI: 10.1016/j.plaphy.2011.01.023
Abstrakt: Galactinol synthase (EC 2.4.1.123; GolS) catalyzes the first step in the synthesis of raffinose family oligosaccharides (RFOs). Their accumulation in response to abiotic stresses implies a role for RFOs in stress adaptation. In this study, the expression patterns of three isoforms of galactinol synthase (CaGolS1-2-3) from Coffea arabica were evaluated in response to water deficit, salinity and heat stress. All CaGolS isoforms were highly expressed in leaves while little to no expression were detected in flower buds, flowers, plagiotropic shoots, roots, endosperm and pericarp of mature fruits. Transcriptional analysis indicated that the genes were differentially regulated under water deficit, high salt and heat stress. CaGolS1 isoform is constitutively expressed in plants under normal growth conditions and was the most responsive during all stress treatments. CaGolS2 is unique among the three isoforms in that it was detected only under severe water deficit and salt stresses. CaGolS3 was primarily expressed under moderate and severe drought. This isoform was induced only at the third day of heat and under high salt stress. The increase in GolS transcription was not reflected into the amount of galactinol in coffee leaves, as specific glycosyltransferases most likely used galactinol to transfer galactose units to higher homologous oligosaccharides, as suggested by the increase of raffinose and stachyose during the stresses.
(Copyright © 2011 Elsevier Masson SAS. All rights reserved.)
Databáze: MEDLINE
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