Glucosamine causes overproduction of reactive oxygen species, leading to repression of hypocotyl elongation through a hexokinase-mediated mechanism in Arabidopsis.
Glucosamine (GlcN) is a naturally occurring amino-sugar that is synthesized by amidation of fructose-6-phosphate. Although a number of reports have examined the biological effects of GlcN on insulin resistance in mammalian systems, little is known about its effects on plant growth. In this study, we have shown that exogenous GlcN inhibits hypocotyl elongation in Arabidopsis, whereas glucose and its analogs alleviate this inhibitory effect. The hexokinase (HXK)-specific inhibitor mannoheptulose also restored hypocotyl elongation. The gin2-1 mutants with an alteration in AtHXK1 exhibited higher tolerance to GlcN. We also found that GlcN induces a significant increase in the production of reactive oxygen species (ROS). In addition, the GlcN-mediated inhibition of hypocotyl elongation was relieved by reducing agents such as ascorbic acid and glutathione. GlcN treatment resulted in significant induction of expression of GST1, GST2 and GST6, which are marker genes for ROS production. The gin2 mutation also represses the ROS production and the GST2 induction by GlcN treatment. Taken together, these results provide evidence that GlcN induces HXK-mediated induction of oxidative stress, leading to growth repression in Arabidopsis thaliana.
Ju
Hyun-Woo
HW
Department of Plant Biotechnology, Agricultural Plant Stress Research Center and Biotechnology Research Institute, College of Agriculture and Life Science, Chonnam National University, Gwangju, Korea.
Koh
Eun-Ji
EJ
Kim
Sun-Hee
SH
Kim
Kang-Il
KI
Lee
Hojoung
H
Hong
Suk-Whan
SW
D017360:Arabidopsis / Q000187:drug effects* / Q000201:enzymology* / Q000235:genetics / Q000254:growth & development; D001205:Ascorbic Acid / Q000494:pharmacology; D003470:Culture Media; D015971:Gene Expression Regulation, Enzymologic / Q000187:drug effects; D018506:Gene Expression Regulation, Plant / Q000187:drug effects; D005944:Glucosamine / Q000494:pharmacology*; D005947:Glucose / Q000031:analogs & derivatives / Q000494:pharmacology; D005978:Glutathione / Q000494:pharmacology; D005982:Glutathione Transferase / Q000235:genetics / Q000378:metabolism; D006593:Hexokinase / Q000037:antagonists & inhibitors / Q000235:genetics / Q000378:metabolism*; D006861:Hydrogen Peroxide / Q000378:metabolism; D018546:Hypocotyl / Q000201:enzymology* / Q000254:growth & development*; D008356:Mannoheptulose / Q000494:pharmacology; D009154:Mutation / Q000235:genetics; D018384:Oxidative Stress / Q000187:drug effects; D017382:Reactive Oxygen Species / Q000378:metabolism*; D019163:Reducing Agents / Q000494:pharmacology; D036226:Seedlings / Q000187:drug effects / Q000201:enzymology / Q000254:growth & development
D003470:Culture Media; D017382:Reactive Oxygen Species; D019163:Reducing Agents; D008356:Mannoheptulose; D006861:Hydrogen Peroxide; D005982:Glutathione Transferase; D006593:Hexokinase; D005978:Glutathione; D005947:Glucose; D005944:Glucosamine; D001205:Ascorbic Acid