Ying-Hui Fu

Ying-Hui Fu (傅嫈惠)
Residence	San Francisco, CA
Spouse(s)	Louis Ptáček
Scientific career
Fields	Neuroscience, Genetics, Neuroscience of sleep
Institutions	UCSF
Website	http://www.neugenes.org/outreach.htm

Ying-Hui Fu (傅嫈惠) is a biologist and human geneticist. Fu is currently a professor of neurology at the University of California, San Francisco. Her work focuses on studying heritable traits in humans, linking them back to DNA mutations, and using animal models to further explore the mechanisms underlying various phenotypes and the heritability of these phenotypes.

In 1980, Fu received a degree in food science from National Chung-Hsing University in Taiwan. In her study of food sciences, she was introduced to biochemistry and microbiology, which led her to study DNA manipulation. She then received her Ph.D. in biochemistry and molecular biology from Ohio State University in 1986. She continued to work at OSU for three more years in a post-doctoral position studying gene regulation in fungi. During her time at OSU, she cloned numerous genes important for nitrogen and sulfur metabolism in Neurospora. One of these genes, cys-3, encodes a leucine zipper protein. It was hypothesized that leucine zippers were DNA-binding elements. The first proof of this in living organisms was a mutation in the cys-3 leucine zipper, which caused a sulfur metabolism defect. After studying the mutation, Fu demonstrated that the mutated cys-3 was unable to bind DNA.

In 1989, Fu transferred to the Baylor College of Medicine as a post-doctoral fellow to study human genetics. While there, she was part of the team that identified the fragile-X syndrome gene. The gene contains a polymorphic CGG trinucleotide repeat in their DNA sequence; the repeat ranged from 6 to 54 in individuals with normal X chromosomes. The transition from stable to unstable occurred between 46 to 52 repeats. The instability increases the likelihood of fragile-X mental retardation. The repeats have a tendency to expand in transmission through meiosis. The size of the repeat correlates with severity of the disease. Fu cloned one of the genes responsible for a form of muscular dystrophy called myotonic dystrophy, and showed that an expanded trinucleotide repeat in this gene also was unstable and caused the disease. Together, these discoveries characterized the molecular basis of genetic “anticipation,” the phenomenon of worsening severity in subsequent generations, as being due to unstable, expanded trinucleotide repeats.

After her postdoc position, Fu worked in biotech industry for four years before returning to academia. She worked first for two years from January 1993 - 1995 at Millennium Pharmaceutical Corporation, a biopharmaceutical company focused on oncology and inflammation (later acquired by Takeda Pharmaceutical Company). After leaving Millennium Pharmaceutical, from 1995- August 1997 Fu worked for Darwin Molecular Corporation for two years and took part in the search for the mutations responsible for premature aging (Werner Syndrome) and early onset Alzheimer's Disease (Presinilin 2).

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