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α-galactosidase-mediated raffinose turnover regulates carbon allocation and vascular patterning of roots during chickpea germination.

Created on 18 Oct 2026

Authors

J J Jenisha, Marcus Samuel, Rex Arunraj

Published in

Physiology and molecular biology of plants : an international journal of functional plant biology. Volume 32. Issue 10. Pages 2309-2318. Epub Sep 30, 2026.

Abstract

Alpha-galactosidase is a hydrolytic enzyme that catalyzes the breakdown of raffinose family oligosaccharides (RFOs), releasing sucrose and galactose for metabolism during germination, development, and under stress. In chickpea (Cicer arietinum L.), RFOs serve as important carbohydrate reserves that support energy supply, phloem transport, and cell wall biosynthesis. This study investigates the effects of deoxygalactonojirimycin (DGJ), a known inhibitor of α-galactosidase, on root anatomy, sugar dynamics, and gene expression to elucidate its role in root development. DGJ-treated chickpea seeds resulted in reduced germination and root elongation. Anatomical analysis exhibited a decrease in root diameter, root cortex area, and vascular bundle area and a reduced number of metaxylem vessels with a difference in the architecture of the vascular bundle. From the sugar profile it is highlighted that RFO accumulated in the developing root tissues, reducing the sucrose and reducing sugar availability. This substantiated that α-galactosidase plays a crucial role in carbohydrate mobilization, vascular patterning, and root tissue development. Furthermore, DGJ-induced sugar stress triggered tissue-specific upregulation of α-galactosidase isogenes across both vascular and non-vascular root tissues, suggesting a coordinated transcriptional response to help restore sugar homeostasis. Collectively, this study uncovered that α-galactosidase plays a key role in the mobilization of RFOs during germination for the early root development.
The online version contains supplementary material available at https://doi.org/10.1007/s12298-026-01829-w.

PMID:
42892778
Bibliographic data and abstract were imported from PubMed on 18 Oct 2026.

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