Factors Affecting the Induction of Lignin Peroxidase in Manganese-Deficient Cultures of the White Rot Fungus Phanerochaete chrysosporium
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Affiliation(s)
1Tel Hai Academic College, Kiryat Shmona, Israel.
2Faculty of Medicine in the Galilee, Bar-Ilan University, Safed, Israel.
3Department of Plant Pathology and Microbiology, The Robert H. Smith Faculty of Agriculture, Food and Environment, The Hebrew University of Jerusalem, Rehovot, Israel.
2Faculty of Medicine in the Galilee, Bar-Ilan University, Safed, Israel.
3Department of Plant Pathology and Microbiology, The Robert H. Smith Faculty of Agriculture, Food and Environment, The Hebrew University of Jerusalem, Rehovot, Israel.
ABSTRACT
The lignin peroxidase (LIP) production and regulation, in manganese ions (Mn2+) deficient cultures of the white rot fungus Phanerochaete chrysosporium, is still not clearly understood. Mn2+
deficiency is correlated to low levels of manganese containing
superoxide dismutase (MnSOD). In this work, we show that despite the low
activity level of MnSOD in Mn2+-deficient cultures, the presence of H2O2 is essential for the expression of the lip-H2 gene, which encodes for the major LIP isoenzyme produced (LIP-H2). Thus, the H2O2 present in Mn2+-deficient
cultures is probably produced by other mechanisms rather than
dismutation of superoxide ions by MnSOD. Glyoxal oxidase gene (glox) expression was significantly higher than MnSOD (MnSOD1) and cellobiose dehydrogenase (cdh1) expression in Mn2+-deficient cultures, indicating its clear involvement in H2O2 production in those cultures. Glyoxal oxidase may compensate the absence of MnSOD activity in Mn2+-deficient cultures. The high levels of reactive oxygen species (ROS) needed for the enhancement of LIP expression in Mn2+-deficient
cultures were not directly correlated to the protein kinase C (PKC)
activity involved in signal transduction pathway. High level of
oxidative stress was observed in MnSOD silenced mutants, grown in the
presence of Mn2+, indicating that oxidative stress in Mn2+-deficient cultures was caused by low levels of MnSOD rather than the deficiency in Mn2+. The results of this work can further contribute to the understanding of LIP regulation in Mn2+-deficient cultures.
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