| Project/Area Number |
26670529
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Dermatology
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| Research Institution | Kyoto University |
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Principal Investigator |
DAINICHI Teruki 京都大学, 医学(系)研究科(研究院), 講師 (20423543)
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| Co-Investigator(Renkei-kenkyūsha) |
HONDA Tetsuya 京都大学, 大学院医学研究科, 准教授 (40452338)
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| Project Period (FY) |
2014-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2014: ¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
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| Keywords | 非対称細胞分裂 / 表皮細胞 / PDK1 / 遺伝子欠損動物 / イメージング |
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| Outline of Final Research Achievements |
The differentiation of the epidermis begins with the stem cells located within the basal layer, and asymmetric cell division (ACD) promotes cell differentiation and organizes the stratified epithelium. However, both the molecular cues that trigger organization of the apical complex during ACD and the signaling pathways that drive activation of apical complex components remain to be defined. We generated mice lacking PDK1 in keratinocytes (PDK1CKO), which display severe defects in epithelial differentiation and stratification resulting in perinatal lethality. ACD in epidermis from PDK1CKO was significantly decreased. Cell-cell contact stimuli induce production of PIP3 at the apical side of basal cells. PDK1 recruits and activates atypical protein kinase C (aPKC). Thus PDK1 regulates both activation and spatial organization of key signaling pathways in response to apical cues acting on basal progenitor cells in developing epidermis.
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