September 20th, Thursday, 2018 2:00-3:00 p.m.
discreteness of cell fates is an inherent and fundamental feature of
multicellular organisms. Here we show that cross-antagonistic mechanisms of
actions of MyoD and PPARg,
which are the master regulators of muscle and adipose differentiation,
respectively, confer robustness to the integrity of cell differentiation.
Simultaneous expression of MyoD and PPARg in
mesenchymal stem/stromal cells led to the generation of a mixture of
multinucle- ated myotubes and
lipid-filled adipocytes. Interest- ingly, hybrid cells (i.e., lipid-filled myotubes)
were not generated, suggesting that these differentiation programs are mutually
exclusive. Mechanistically, although exogenously expressed MyoD was
rapidly degraded in adipocytes through ubiquitin-protea- some pathways, exogenously expressed PPARg was
not downregulated in myotubes. In PPARg-
expressing myotubes, PPARg-dependent
histone hyperacetylation was
inhibited in a subset of adipo-
genic gene loci, including that of C/EBPa, an essen- tial effector of PPARg.
Thus, the cross-repressive interactions between MyoD- and PPARg-induced differentiation programs ensure
discrete cell-fate decisions.
majority of my research experience has been focused on understanding the
molecular mechanism of skeletal muscle stem cells, as well as their
self-renewal, proliferation and differentiation. My previous education and
research experience provided me with a strong background in stem cell biology.
As an undergraduate student, I mastered some theoretical knowledge of stem cell
biology. As a graduate student, in the area of muscle development, aimed to
understand how extracellular gene is involved in muscle stem cell’s
self-renewal, proliferation and differentiation, and found that semaphorin-3A,
an axon guidance protein, secreted form muscle stem cells and promotes their
proliferation and differentiation capability by regulation of their master
regulator genes expression. Currently, as a postdoctoral fellow in the Asakura lab
at University of Minnesota, I am working on the direct lineage reprogramming of
mouse embryonic fibroblasts(MEFs) into myogenic cells. The repair of skeletal
muscle needs a sufficient number of myogenic cells to replace the damaged
tissue, therefore, expansion of cells is generally required. Myogenic cells
derived by direct-reprogramming may provide a solution to the limitations of
current stem cell-based therapy of muscular dystrophy. Throughout the course of
my research experience, I served as the primary or co-investigator in all of my
studies. Based on my previous work, I have a strong understanding of the
fundamental concepts of muscular stem cells. My dedication and experience in
stem cell biology makes me a strong candidate for this application and would
allow me to continue contributing to this field of research.
Professors and students of TBSI are welcome to attend. The lecture is also open to the public. For off-campus personnel, please scan the QR code and and fill in your information (name, company, contact number, ID number). The language of the lecture is English.