| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2017: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2016: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Outline of Final Research Achievements |
Our previous study revealed that the local loss of cells resulting from tissue damage triggers sporadic cellular hypertrophy to repair the tissue. This ‘‘compensatory cellular hypertrophy’’ (CCH) is implemented by polyploidization through acceleration of the endocycle, a variant cell cycle composed of DNA synthesis and gap phases without mitosis.
As a physiological model of CCH, we used the Drosophila ovarian stretched-follicle cells in which cellular stretch-induced extra endocycle and endogenous activation of the IIS are observed during their development. In this study, we found that a transient receptor potential channel (TRPC) is involved in both the physiological CCH and the damage-induced CCH in the follicle epithelia. Further functional analyses of the TRPC in the follicle cells led us to conclude that TRPC activation in response to mechanical stretching stress induces calcium incorporation, thereby activating IIS pathway to accelerate endocycling during CCH.
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