Premium
Myo‐inositol oxygenase is important for the removal of excess myo‐inositol from syncytia induced by H eterodera schachtii in A rabidopsis roots
Author(s) -
Siddique Shahid,
Endres Stefanie,
Sobczak Miroslaw,
Radakovic Zoran S.,
Fragner Lena,
Grundler Florian M. W.,
Weckwerth Wolfram,
Tenhaken Raimund,
Bohlmann Holger
Publication year - 2014
Publication title -
new phytologist
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.742
H-Index - 244
eISSN - 1469-8137
pISSN - 0028-646X
DOI - 10.1111/nph.12535
Subject(s) - heterodera schachtii , inositol , biochemistry , mutant , syncytium , glucuronate , biology , inositol phosphate , arabidopsis , oxygenase , chemistry , gene , nematode , cell , receptor , ecology
Summary The enzyme myo‐inositol oxygenase is the key enzyme of a pathway leading from myo‐inositol to UDP ‐glucuronic acid. In A rabidopsis, myo‐inositol oxygenase is encoded by four genes. All genes are strongly expressed in syncytia induced by the beet cyst nematode H eterodera schachtii in A rabidopsis roots. Here, we studied the effect of a quadruple myo‐inositol oxygenase mutant on nematode development. We performed metabolite profiling of syncytia induced in roots of the myo‐inositol oxygenase quadruple mutant. The role of galactinol in syncytia was studied using A rabidopsis lines with elevated galactinol levels and by supplying galactinol to wild‐type seedlings. The quadruple myo‐inositol oxygenase mutant showed a significant reduction in susceptibility to H . schachtii , and syncytia had elevated myo‐inositol and galactinol levels and an elevated expression level of the antimicrobial thionin gene T hi2.1 . This reduction in susceptibility could also be achieved by exogenous application of galactinol to wild‐type seedlings. The primary function of myo‐inositol oxygenase for syncytium development is probably not the production of UDP ‐glucuronic acid as a precursor for cell wall polysaccharides, but the reduction of myo‐inositol levels and thereby a reduction in the galactinol level to avoid the induction of defence‐related genes.