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2, Regulation of cell number and size of tissue via programmed cell death mechanism A developing animal is exposed to both intrinsic and extrinsic stresses. Even in these stressful environmental conditions, animal development is achieved with the surprisingly robust patterns. We thought that stress response in developing animal is a key for the regulation of robustness of development. One important stress response will be caspase activation. Caspase activation is not only observed in apoptosis but also in non apoptotic condition. Non apoptotic caspase function includes cell proliferation, migration and differentiation. We are studying the roles of caspases that play crucial roles for developmental robustness. Cell number of the tissue is tightly regulated and this regulation is crucial for homeostatic maintenance of the body. Regulatory mechanisms of the tissue quorum are thought to be based on the communication between dying cells and proliferating cells in whole body. We are investigating the basic mechanisms of the tissue quorum control not only in the tissue but also in whole body.

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Energy metabolism underlies all of the biological activities. Recent studies have shown that several biological events such as cancer growth, infection, or development accompany changes of energy metabolism at cellular and organismal levels. These observations suggest importance of controlling energy metabolism to meet the demands of each biological event, but it remains unclear yet how the control of energy metabolism is coupled with cell death, development, and growth. We have revealed how energy metabolism is reorganized during early mouse development by exhaustive metabolomics analysis and gene expression analysis. References Miyazawa, H., Yamaguchi, Y., Sugiura, Y., Honda, K., Kondo, K., Matsuda, F., Yamamoto, T., Suematsu, M., and Miura, M.: Rewiring of embryonic glucose metabolism via suppression of PFK-1 and aldolase during mouse chorioallantoic branching. Development 144, 63-73, 2017. doi:10.1242/dev.138545 Back to Research page

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