Repository logo
Log In(current)
  1. Home
  2. Prodotti della ricerca
  3. A. Contributo su rivista
  4. A1. Articolo in rivista
  5. A metabolic profiling analysis revealed a primary metabolism reprogramming in Arabidopsis glyI4 loss-of-function mutant

A metabolic profiling analysis revealed a primary metabolism reprogramming in Arabidopsis glyI4 loss-of-function mutant

Author(s)
Proietti, Silvia  
Bertini, Laura  
Falconieri, Gaia Salvatore
Baccelli, Ivan
Timperio, Anna Maria  
more
Date Issued
2021
Type
article
Volume
10
Issue
11
Start Page
2464
DOI
10.3390/plants10112464
Journal
PLANTS  
Abstract
Methylglyoxal (MG) is a cytotoxic compound often produced as a side product of metabolic processes such as glycolysis, lipid peroxidation, and photosynthesis. MG is mainly scavenged by the glyoxalase system, a two-step pathway, in which the coordinate activity of GLYI and GLYII transforms it into D-lactate, releasing GSH. In Arabidopsis thaliana, a member of the GLYI family named GLYI4 has been recently characterized. In glyI4 mutant plants, a general stress phenotype characterized by compromised MG scavenging, accumulation of reactive oxygen species (ROS), stomatal closure, and reduced fitness was observed. In order to shed some light on the impact of gly4 loss-of-function on plant metabolism, we applied a high resolution mass spectrometry-based metabolomic approach to Arabidopsis Col-8 wild type and glyI4 mutant plants. A compound library containing a total of 70 metabolites, differentially synthesized in glyI4 compared to Col-8, was obtained. Pathway analysis of the identified compounds showed that the upregulated pathways are mainly involved in redox reactions and cellular energy maintenance, and those downregulated in plant defense and growth. These results improved our understanding of the impacts of glyI4 loss-of-function on the general reprogramming of the plant’s metabolic landscape as a strategy for surviving under adverse physiological conditions.
Handle
http://hdl.handle.net/2067/46276
Metrics

Built with DSpace-CRIS software - Extension maintained and optimized by 4Science

  • Accessibility settings
  • Privacy policy
  • End User Agreement
  • Send Feedback
Repository logo COAR Notify