| Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2015: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2014: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2013: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
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| Outline of Final Research Achievements |
It has been reported that an ADAMTS9 gene variant is associated with type 2 diabetes. The underlying pathology of type 2 diabetes is insulin resistance and beta-cell dysfunction. However, the molecular mechanisms underlying ADAMTS9 function in beta cells and peripheral tissues are unknown.
We investigated whether GON-1, the C.elegans homolog of ADAMTS9, is involved in the insulin secretion and insulin signaling in C.elegans. We found that both insulin secretion and the insulin-signaling pathway are compromised by GON-1 depletion. These defects in gon-1 mutants were restored by GON domain expression. These data suggest that the GON domain of GON-1 is involved in protein secretion from insulin secretory cells and in insulin/IGF-like signaling at peripheral tissues.
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