| Budget Amount *help |
¥3,300,000 (Direct Cost: ¥3,300,000)
Fiscal Year 2005: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 2004: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 2003: ¥1,900,000 (Direct Cost: ¥1,900,000)
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| Research Abstract |
This study aims to elucidate the signaling mechanism of sexual development of basidiomycetous mushrooms from mating to fruit body formation. Here, stimulation factors for sexual development of the model basidiomycete, Schizophyllum commune, were researched from both viewpoints of environmental factors (external signal factors) and genetic factors.
1. Environmental factors (external signal factors)
Effects of external signal factors on fruit body formation of S.commune were examined by addition of indole-related compounds to agar media. At the low concentration of 100μg/ml, effects on fruit body formation of indole (Ind), 3-indoleacetic acid (IAA), 3-indolecarboxylic acid (ICA), 3-indolepropionic acid (IPA) and tryptophan (Trp) were as follows : IBA>ICA≧IPA≧IAA>Ind≧Trp. This result showed that compounds containing a structural moiety of indole stimulated fruit body formation.
2. Genetic factors
Trp-systhesizing gene of S.commune, TRP1, suppresses abnormality in sexual development (abnormal mating and nuclear migration) induced by indole-resistant mutation (ind1) and caffeine-resistant mutation (cfn1). Sequencing analysis of the TRP1 showed that its product was an enzyme with three catalytic regions. One of the three regions, IGPS (indole-3-glycerol phosphate synthetase) had ability to suppress the abnormal sexual development. Therefore, highly expressed IGPS gene was constructed, and dikaryon with high expression of IGPS was made using the IGPS gene constructed. The dikaryon with high expression of IGPS formed fruit bodies 10 days earlier than dikaryons with no or usual expression of IGPS externally introduced. This result showed that the IGPS region in TRP1 had ability to stimulate sexual development of wild-typed strains as well as the ability to suppress abnormal sexual development of ind1 and cfn1 mutant strains.
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