title: The changes in pectin metabolism in flax infected with Fusarium.
abstract: Fusarium culmorum and Fusarium oxysporum are the most common fungal pathogens of flax (Linum usitatissimum L.), thus leading to the greatest losses in crop yield. A subtractive cDNA library was constructed from flax seedlings exposed for two days to F. oxysporum. This revealed a set of genes that are potentially involved in the flax defense responses. Two of those genes directly participate in cell wall sugar polymer metabolism: UDP-D-glucuronate 4-epimerase (GAE; EC 5.1.3.6) and formate dehydrogenase (FDH; EC 1.2.1.2). GAE delivers the main substrate for pectin biosynthesis, and decreases were detected in its mRNA level after Fusarium infection. FDH participates in the metabolism of formic acid, and the expression level of its gene increased after Fusarium infection. However, metabolite profiling analysis disclosed that the pectin content in the infected plants remained unchanged, but that there were reductions in both the levels of the soluble sugars that serve as pectin precursors, and in the level of formic acid. Since formic acid is the product of pectin demethylesterification, the level of mRNAs coding for pectin methylesterase (EC 3.1.1.11) in the infected flax was measured, revealing a decrease in its expression upon plant infection. Transgenic flax plants overexpressing fungal polygalacturonase (EC 3.2.1.15) and rhamnogalacturonase (EC 3.2.1.-) showed a decrease in the pectin content and an elevated level of formic acid, but the level of expression of the FDH gene remained unchanged. It is suspected that the expression of the formate dehydrogenase gene is directly controlled by the pathogen in the early stage of infection, and additionally by pectin degradation in the later stages.
authors: Faculty of Biotechnology, University of Wroclaw, Przybyszewskiego 63/77, 51-148 Wroclaw, Poland.
authors: Wioleta
authors: W
authors: Wojtasik
authors: Anna
authors: A
authors: Kulma
authors: Kamil
authors: K
authors: Kostyn
authors: Jan
authors: J
authors: Szopa
mesh_terms: D000596:Amino Acids / Q000378:metabolism; D002238:Carbohydrate Epimerases / Q000235:genetics / Q000378:metabolism; D050260:Carbohydrate Metabolism; D002265:Carboxylic Ester Hydrolases / Q000235:genetics / Q000378:metabolism; D018076:DNA, Complementary; D019597:Flax / Q000235:genetics / Q000378:metabolism* / Q000382:microbiology*; D005560:Formate Dehydrogenases / Q000235:genetics / Q000378:metabolism; D005561:Formates / Q000378:metabolism; D005670:Fusarium / Q000472:pathogenicity*; D018506:Gene Expression Regulation, Plant; D006026:Glycoside Hydrolases / Q000235:genetics / Q000378:metabolism; D054884:Host-Pathogen Interactions; D010205:Pantothenic Acid / Q000378:metabolism; D010368:Pectins / Q000378:metabolism*; D010935:Plant Diseases / Q000382:microbiology*; D030821:Plants, Genetically Modified; D011096:Polygalacturonase / Q000235:genetics / Q000378:metabolism; D012333:RNA, Messenger; D036226:Seedlings / Q000382:microbiology / Q000502:physiology
chemical_list: D000596:Amino Acids; D018076:DNA, Complementary; D005561:Formates; D012333:RNA, Messenger; C030544:formic acid; D010205:Pantothenic Acid; D010368:Pectins; D005560:Formate Dehydrogenases; D002265:Carboxylic Ester Hydrolases; C022323:pectinesterase; D006026:Glycoside Hydrolases; C067959:rhamnogalacturonase A; D011096:Polygalacturonase; D002238:Carbohydrate Epimerases; C023258:UDPglucuronate 4-epimerase