报告题目：Hippo-YAP/TAZ signaling regulates cell plasticity to maintain tissue homeostasis.
报告人：Dae-sik Lim 教授
主持人：赵斌 教授
时 间：2025年6月19日（周四）下午4点
地 点：纳米楼457报告厅
报告人简介：
During graduate studies, Dae-sik Lim investigated the function of two genes, Rad51 and Ku80, in the repair of DNA damage in mice. As a postdoctoral researcher under the guidance of Dr. Michael B. Kastan at Johns Hopkins Hospital and St. Jude Children’s Research Hospital in the USA, Prof. Lim identified numerous substrates for ATM—the master kinase gene mutated in ataxia-telangiectasia—and characterized ATM’s role in the DNA damage response pathway. Prof. Lim’s findings were published in leading journals, including Science (1998), PNAS (1999), JBC (1999), Nature (2000), and Nature Reviews Molecular Cell Biology (2000).
In 2000, Prof. Lim began the academic career as an Assistant Professor at Korea University. Dae-sik Lim later joined KAIST as an Assistant Professor (2002–2004), was promoted to Associate Professor (2004–2009), and became a full-time tenured Professor in 2010. From 2010 to 2017, Prof. Lim served as the Director of the National Creative Research Initiative Center for Cell Division and Differentiation. Between September 2017 and May 2019, Prof. Lim held the position of Vice Minister for Science, Technology, and Innovation in the Korean Government, leading initiatives such as the establishment of the National R&D Innovation Plan, allocation and adjustment of national R&D budgets, and evaluation of national R&D projects.
Since returning to KAIST, Prof. Lim has focused on understanding the YAP-induced cell plasticity phenomenon in lung, liver, intestine, and fat tissues. The current research involves identifying and characterizing newly emerging intermediate/transitional cells induced by YAP activation in vivo, with the ultimate goal of uncovering the underlying molecular mechanisms.
Abstract：
The Hippo-YAP/TAZ signaling pathway is a critical developmental program that regulates the growth and division of adult stem/progenitor cells, the size of organs, and the ability of tissues to regenerate. Studies have demonstrated that the activation of YAP typically results in the excessive growth of precursor cells, suppression of differentiation, increased proliferation of neighboring cells, and the development of cancer. Nevertheless, the precise function of this pathway in controlling alterations in cell fate or cell adaptability during tissue regeneration has not been completely understood in living organisms. Recent findings indicate that when YAP is activated in certain cell types, it induces dedifferentiation and transdifferentiation of precursor cells rather than excessive cell proliferation. Initial data suggest that YAP may endow specific types of differentiated cells in multiple tissues with cell plasticity. For example, continuous activation of YAP/TAZ in lung secretory cells leads to cellular reprogramming, causing these cells to lose their original identity and transform into squamous alveolar type 1 (AT1) cells via a specific transitional cell state termed Damage-Associated Transient Progenitors (DATPs). Similarly, continuous activation of YAP/TAZ in mature adipocytes drives their reversion to a less specialized state resembling adipose progenitor cells that express progenitor-associated markers. This discussion focuses on how Hippo-YAP/TAZ signaling influences the fate dynamics of stem/progenitor cells in the lung and adipose tissue, as well as how YAP confers cell plasticity to specific differentiated cell populations.
