by Keith Hautala
(Oct. 1, 2014) — Helen Blau, director of Stanford University's Baxter Laboratory for Stem Cell Biology, will deliver the sixth annual Thomas Hunt Morgan Lecture, presented by the University of Kentucky Department of Biology.
Blau's lecture, titled "Reprogramming Stem Cell Fate and Function," will take place at 4 p.m. on Thursday, Oct. 2, in Room 116 of the Thomas Hunt Morgan Building. Blau will give a second talk, "Extended Healthspan Through Regenerative Medicine," at 10 a.m. on Friday, Oct. 4, in the William T. Young Library Auditorium.
Blau’s research is focused on the regulation of cell fate. In the 1980s her lab challenged and changed the dogma that the mammalian differentiated state was "terminal," i.e., fixed and irreversible.
The Blau lab fused cells of two different species in different ratios to form stable non-dividing syncytia (heterokaryons). These experiments demonstrated that by altering the balance of cytoplasmic proteins, programs of gene expression could be changed. For example, the genes characteristic of a muscle cell could be activated in a human liver cell.
This body of work was remarkable, as it showed that genes silenced in the course of differentiation and development in humans,could be readily reawakened and expressed. Moreover, these major changes in gene expression occurred in the absence of cell division and DNA replication.
These findings surprised the scientific community by showing that in mammals the typically stable state of a differentiated cell — liver does not normally beget muscle — is governed by mechanisms that are continuously active and governed by the balance of proteins present in the cytoplasm at any given time.
These discoveries extended the findings and fundamental principles of gene regulation described for the Operon in prokaryotes by Jacob and Monod to higher eukaryotes. Moreover, they now provide the foundation for the diverse approaches to nuclear reprogramming that are the crux of the burgeoning field of stem cell biology and regenerative medicine.