| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2001: ¥1,300,000 (Direct Cost: ¥1,300,000)
Fiscal Year 2000: ¥2,200,000 (Direct Cost: ¥2,200,000)
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| Research Abstract |
Multicellular organisms have developed a wide array of intercellular communication mediated through various signaling molecules. Therefore, we attempted to identify signaling molecules in such intercellular communication. We particularly focused on the phenomenon where one of the aggregation defective mutants, erk2-null, can be rescued by mixing with wild type cells. We found that wild type cells secrete low molecular weight lipophilic signaling molecules capable of restoration of erk2-null development (Maeda and Kuwayama, 2000). We also revealed that DIP-1, differentiation inducing factor of stalk cell, rescued the morphogenesis of erk2-null (Kuwayama et al., 2000). Recently, however, the mutant (HM1030) defective in DIF-1 synthesis that was created by Dr. R. Kay lab still retained the activity to rescue erk2-null. Currently, we are purifying low molecular weight lipophilic molecules secreted by HM1030. After HPLC and ESI-MS, the, molecular weight of the putative factor is 249.9.
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