CURRICULUM VITAE
Name:
Yi-der Chen
Business Address: Mathematical Research Branch, National Institute
of Diabetes and
Digestive and Kidney Diseases, National
Institutes of Health,
Bethesda, MD 20892-2690.
Present Job Title: Research Chemist
Phone Number: 301-496-5436 (phone)
301-402-0535 (fax)
Date of Birth: May 29,1940.
Marital Status: Married with two children.
Education and Degree:
B.S.,
National Taiwan University, Taipei, Taiwan. Chemical Engineering (1963).
M.S.,
National Tsing Hua University, Hsin Chu, Taiwan. Chemistry (1965).
Ph.D.,
Pennsylvania State University, University Park, Pa. Chemistry (1969)
Professional Experience:
Research
Chemist, Mathematical Research Branch, NIDDK,
National Institutes of Health, Sept., 1997-present.
Visiting
Professor, Department of Biochemistry, The Hong Kong University
of Science and Technology, May-July, 1993, May
1995.
Research
Chemist, Laboratory of Molecular Biology, NIDDK, National Institutes
of Health, July 1978- Sept. 1997.
Visiting
Scientist, Laboratory of Molecular Biology, NIDDK, National
Institutes
of Health, 1972-1978.
Research
Chemist, Division of Natural Sciences, University of California
at Santa Cruz, 1969-1972.
General Research Interests:
(1). Free Energy Transduction in Biology: Active Transport Across Membranes,
Fluctuation Induced Active Transport, Directional Movement of Brownian Particles
in a Fluctuating Potential Field, Kinesin Movement on Microtubule, Muscle
Contraction, Flagella Motor Rotation.
(2). Theoretical Modeling and Application of Statistical Mechanics and Thermodynamics
in Biology: Equilibrium and Kinetic Studies of Binding of One or More
Ligands to Linear Biopolymers, Treadmilling and Phase Instability in Microtubule
Aggregation, Theory of Noise and Fluctuation in Biological Systems, Theory
of Protein Folding.
Current research projects:
(1). Theoretic formalism for kinesin motility: In this project, we formulate
mathematical formalisms connecting the biochemical mechanisms of kinesin
motors and the mechanical movement of the bead measured in a typical motility
assay. The purpose is to provide a method to quantitatively assess or differentiate
between various biochemical kinetic models for kinesin motors based on mechanical
data measured in motility assays. In motility assays, it is the movement
of the bead, not the movement of the kinesin, that is directly measured.
Therefore, the mechanical data obtained in motility assays can not be directly
used to elucidate the kinetic mechanism of kinesin movement on microtubule.
We have finished the derivation of the formalism for the case that the kinesin
motor used to move the bead in the motility assay is one-headed. Currently,
we are extending the formulation to two-headed kinesins.
(2). Molecular dynamics simulations of kinesin molecules and kinesin-tubulin
complexes: In this project, we investigate the molecular conformations of
kinesin motors in different nucleotide states using “Molecular Dynamics
Simulation” method. The purpose is to examine how the ATP hydrolysis
reaction at the catalytic site of the motor is coupled to the translocation
of the motor on the microtubule. That is, we are interested in the “molecular
mechanism” of free energy transduction. It is obvious that the generation
of force and the translocation of a kinesin motor on a mirotubule depend
on the nucleotide state of the motor. How the information at the catalytic
site is transmitted to the microtubule binding site and the “lever’
arm site is an interesting but difficult question. Molecular dynamics simulation
is a useful tool to study the molecular basis of this information transmission.
Simulations on kinesin motors in the absence of microtubule showed that both
the motor core and the linker region (the lever arm) change their conformations
according to the bound nucleotide. We are extending the study to including
the microtubule in the simulation.
(3). Theoretical modeling on muscle contraction regulation: In this project,
we carry out a theoretical calculation on the kinetics of binding myosin
sub-fragment 1 to regulated actin for two different muscle regulation models:
the two-state Hill model ( Hill, Eisenberg, and Green, 1980. PNAS 77: 3186-90)
and the three-state Geeves model (McKillop and Geeves, 1993, Biophys. J.
65:693-701). The purpose of this study is to examine whether the Hill model
can account for kinetic binding data, specifically for the ‘lag’
found in the kinetic binding curves when excess S1 binds to regulated actin
filaments in the absence of calcium. It had been claimed before that the
two-state Hill model is unable to account for such a lag. Thus, an alternative
three-state Geeves model was proposed and claimed to be essential for fitting
the lag phase. Here we show that the Hill model can account for the lag in
the kinetic binding data at least as well as the Geeves model. We further
show that both models are indistinguishable in their ability/inability to
account for existing kinetic and equilibrium binding data. Thus, the Hill
model cannot be ruled out on the basis of existing kinetic and equilibrium
binding data.