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.