| Budget Amount *help |
¥84,900,000 (Direct Cost: ¥84,900,000)
Fiscal Year 2008: ¥19,700,000 (Direct Cost: ¥19,700,000)
Fiscal Year 2007: ¥19,700,000 (Direct Cost: ¥19,700,000)
Fiscal Year 2006: ¥19,700,000 (Direct Cost: ¥19,700,000)
Fiscal Year 2005: ¥12,900,000 (Direct Cost: ¥12,900,000)
Fiscal Year 2004: ¥12,900,000 (Direct Cost: ¥12,900,000)
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| Research Abstract |
We identified a distinct type of ER-derived structure as a new organelle in Arabidopsis, which we have designated the ER body. The spindle-shaped, 5-10 μm long ER bodies are easily detected in Arabidopsis expressing ER-targeted GFP. ER bodies are uniformly distributed throughout the epidermis of cotyledons and hypocotyls in young seedlings. Interestingly, wounding or treatment with the wound hormone jasmonate induces the accumulation of ER bodies in adult leaves. This suggests that the ER body is involved in pest/pathogen resistance in Arabidopsis. The ER bodies in Arabidopsis seedlings accumulate PYK10 protein, which bears the ER retention signal KDEL. The Arabidopsis nai1 mutant lacks ER bodies. The NAI1 gene encodes a basic helix-loop-helix-type transcription factor. NAI1 regulates the expression of PYK10, JAL22, JAL23, JAL31, JAL33, PBP1/JAL30, GLL2 and GLL25. PYK10 forms a large complex with JALs and GLLs in cells that are disrupted. JALs and GLLs regulate the size of the PYK10 complex and may regulate its substrate specificity. As NAI1 deficiency causes the loss of ER bodies, NAI1 may regulate unknown factors that are responsible for the formation of the ER body.
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