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포항공과대학교 생명과학과

ENG

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세미나

Systematic Analysis of Chemotaxis and Cell Cycle Commitment Mechanism

2016-03-04 2039
세미나 일시
2016.3.8(화) 오후2:00
연사
Hee Won Yang, Ph.D.
장소
PBC 179호
[BK21 Plus Seminar] ▶Subject: Systematic Analysis of Chemotaxis and Cell Cycle Commitment Mechanism ▶Speaker: Hee Won Yang, Ph.D. (Postdoctoral Fellow, Department of Chemical and Systems Biology, Stanford University) ▶Date: 2:00 PM/Mar. 8(Tue.)/2016 ▶Place: Conference room(#179), Postech Biotech Center *Abctract Using systematic techniques developed by myself and others, I have been investigating both neutrophil chemotaxis and mammalian cell cycle commitment mechanisms. Neutrophils and other immune cells use amoeboid movement and chemotaxis to reach sites of infection and inflammation. This process requires a polarization mechanism that directs actin polymerization, membrane protrusion and adhesion formation to the cell front. While Ras, Rac, Cdc42, and RhoA small GTPases all regulate chemotaxis, it has not yet been established how they spatially and temporally control polarization and steering. Using fluorescent biosensors and light-inducible gradients of chemoattractant, upon stimulation we find that Cdc42 activity polarizes rapidly, antagonizes RhoA, and maintains a steep spatial gradient during migration, while Ras and Rac polarize later forming shallow gradients. Mammals rely on cell proliferation to orchestrate immune responses, repair tissues and maintain organ size. Understanding the termination of proliferation is an important problem as most cancers require misregulation of signaling pathways that limit cell proliferation. After each cell cycle, proliferating cells have two distinct fates after they complete mitosis when they decide to either rampup cyclin-dependent kinase2 (Cdk2) activity and enter the next cell cycle or suppress Cdk2 activity and exit the cell cycle. It is not yet understood how cells make this critical decision. I combine live single cell imaging with fixed cell immunofluorescence measurement to show that Cdk2 activity bifurcates after mitosis. Systematic analysis and measurement of single cell variation in mitogen and stress signals revealed that integration of these two signals controls cell cycle commitment. Further immunofluorescent measurements after live cell imaging show that competing growth and stress signals are integrated during the preceding cell cycle to promote cell cycle progression. These systematic approaches have allowed me to identify complicated pathways and the genes responsible for both neutrophil chemotaxis and cell cycle commitment. ▶Inquiry: Prof. Sung Ho Ryu (279-2292) * This seminar will be given in Korean. please refrain from taking photos during seminars. *