Phosphoglucose Isomerase Plays a Key Role in Sugar Homeostasis, Stress Response, and Pathogenicity in Aspergillus flavus

Aspergillus flavus is one of the important human and plant pathogens causing not only invasive aspergillosis in immunocompromised patients but also crop contamination resulting from carcinogenic aflatoxins (AFs). Investigation of the targeting factors that are involved in pathogenicity is of unmet need to dismiss the hazard. Phosphoglucose isomerase (PGI) catalyzes the reversible conversion between glucose-6-phosphate and fructose-6-phosphate, thus acting as a key node for glycolysis, pentose phosphate pathway, and cell wall biosynthesis in fungi. In this study, we constructed an A. flavus pgi deletion mutant, which exhibited specific carbon requirement for survival, reduced conidiation, and slowed germination even under optimal experimental conditions. The Δpgi mutant lost the ability to form sclerotium and displayed hypersusceptibility to osmotic, oxidative, and temperature stresses. Furthermore, significant attenuated virulence of the Δpgi mutant was documented in the Caenorhabditis elegans infection model, Galleria mellonella larval model, and crop seeds. Our results indicate that PGI in A. flavus is a key enzyme in maintaining sugar homeostasis, stress response, and pathogenicity of A. flavus. Therefore, PGI is a potential target for controlling infection and AF contamination caused by A. flavus.

Cytosolic phosphofructokinases are important for sugar homeostasis in leaves of Arabidopsis thaliana

Background and Aims ATP-dependent phosphofructokinases (PFKs) catalyse phosphorylation of the carbon-1 position of fructose-6-phosphate, to form fructose-1,6-bisphosphate. In the cytosol, this is considered a key step in channelling carbon into glycolysis. Arabidopsis thaliana has seven genes encoding PFK isoforms, two chloroplastic and five cytosolic. This study focusses on the four major cytosolic isoforms of PFK in vegetative tissues of A. thaliana. Methods We have isolated homozygous knock-out individual mutants (pfk1, pfk3, pfk6, pfk7) and two double mutants (pfk1/7 and pfk3/6) and characterized their growth and metabolic phenotypes. Key Results In contrast to single mutants and the double mutant pfk3/6 for the hypoxia-responsive isoforms, the double mutant pfk1/7 had reduced PFK activity and shows a clear visual and metabolic phenotype with reduced shoot growth, early flowering, and elevated hexose levels. This mutant also has an altered ratio of short/long aliphatic glucosinolates and an altered root-shoot distribution. Surprisingly, this mutant does not show any major changes in short-term carbon flux and in levels of hexose-phosphates. Conclusions We conclude that the two isoforms PFK1 and PFK7 are important for sugar homeostasis in leaf metabolism and apparently source/sink relations in Arabidopsis, while PFK3 and PFK6 only play a minor role under normal growth conditions.