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Physiological aspects of raffinose family oligosaccharides in plants: protection against abiotic stress
Faculty
Agriculture
Year:
2014
Type of Publication:
Article
Pages:
1-8
Authors:
ElSayed, A. I, Rafudeen, M. S, Golldack, D
DOI:
10.1111/plb.12053
Journal:
PLANT BIOLOGY WILEY-BLACKWELL
Volume:
16
Research Area:
Plant Sciences
ISSN
ISI:000328826900001
Keywords :
Abiotic stress, galactinol synthase, myo-inositol, raffinose
Abstract:
Abiotic stresses resulting from water deficit, high salinity or periods of drought adversely affect plant growth and development and represent major selective forces during plant evolution. The raffinose family oligosaccharides (RFOs) are synthesised from sucrose by the subsequent addition of activated galactinol moieties donated by galactinol. RFOs are characterised as compatible solutes involved in stress tolerance defence mechanisms, although evidence also suggests that they act as antioxidants, are part of carbon partitioning strategies and may serve as signals in response to stress. The key enzyme and regulatory point in RFO biosynthesis is galactinol synthase (GolS), and an increase of GolS in expression and activity is often associated with abiotic stress. It has also been shown that different GolS isoforms are expressed in response to different types of abiotic stress, suggesting that the timing and accumulation of RFOs are controlled for each abiotic stress. However, the accumulation of RFOs in response to stress is not universal and other functional roles have been suggested for RFOs, such as being part of a carbon storage mechanism. Transgenic Arabidopsis plants with increased galactinol and raffinose concentrations had better ROS scavenging capacity, while many sugars have been shown in vitro to have antioxidant activity, suggesting that RFOs may also act as antioxidants. The RFO pathway also interacts with other carbohydrate pathways, such as that of O-methyl inositol (OMI), which shows that the functional relevance of RFOs must not be seen in isolation to overall carbon re-allocation during stress responses.
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