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Dr Chieh Hsu

Eastern ARC Research Fellow

School of Biosciences

 

Chieh did his BSc studies in National Taiwan University in 2002. He continued his postgraduate studies in the Molecular Biology Program, University of Goettingen, Germany, and received MSc in Biochemistry mentored by Dr Jobst Landgrebe (2004-2006). He developed strong interest in cell biology and contributed to the early findings in exosome biogenesis during his PhD curriculum in Prof Mikael Simons' lab at the Max-Planck Institute for Experimental Medicine (2006-2010). Later he broadened his research interest into molecular systems biology. He joined Prof Attila Becskei's group in University of Zurich (2010-2011) and University of Basel (Biozentrum, 2011-2015), Switzerland and was awarded the long-term fellowship from Human Frontier Science Program (2011-2014) to study system stability, cellular memory, and stochastic/deterministic factors in transcriptional auto-regulatory circuits.

Chieh joined School of Biosciences as the Eastern ARC Research Fellow in synthetic biology in March 2015. He aims to bridge disciplines for quantitative studies on intracellular membrane trafficking.

Location:

Room: S103B
Ext: 16474
Lab: S110/S125
Ext: 3742/3585
Email: C.Hsu@kent.ac.uk

ORCID ID:0000-0002-4780-1222

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Also view these in the Kent Academic Repository

Article
Jaquet, V., Hsu, C. and Becskei, A. (2017). Measurement of bistability in a multidimensional parameter space. Integrative Biology [Online] 9:167-177. Available at: http://dx.doi.org/10.1039/C6IB00242K.
Hsu, C. et al. (2016). Protein dimerization generates bistability in positive feedback loops. Cell reports [Online] 16:1204-1210. Available at: http://dx.doi.org/10.1016/j.celrep.2016.06.072.
Hsu, C. et al. (2016). Contribution of bistability and noise to cell fate transitions determined by feedback opening. Journal of Molecular Biology [Online]. Available at: http://dx.doi.org/10.1016/j.jmb.2016.07.024.
Hsu, C. et al. (2012). Stochastic signalling rewires the interaction map of a multiple feedback network during yeast evolution. Nature communications [Online] 3:Article 682. Available at: http://dx.doi.org/10.1038/ncomms1687.
Prenzel, T. et al. (2011). Estrogen-dependent gene transcription in human breast cancer cells relies upon proteasome-dependent monoubiquitination of histone H2B. Cancer research [Online] 71:5739-5753. Available at: http://dx.doi.org/10.1158/0008-5472.CAN-11-1896.
Hsu, C. et al. (2010). Regulation of exosome secretion by Rab35 and its GTPase-activating proteins TBC1D10A-C. The Journal of cell biology [Online] 189:223-232. Available at: http://dx.doi.org/10.1083/jcb.200911018.
Trajkovic, K. et al. (2008). Ceramide triggers budding of exosome vesicles into multivesicular endosomes. Science (New York, N.Y.) [Online] 319:1244-1247. Available at: http://www.sciencemag.org/content/319/5867/1244.
Total publications in KAR: 7 [See all in KAR]
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We are currently establishing two major synthetic frameworks using the yeast Saccharomyces cerevisiae:

  1. Positive feedback loops and protein membrane domains. In eukaryotic cells, organelles exchange materials in membranous vesicles in a process called intracellular membrane trafficking. To ensure proper sorting, a given membrane needs to be identified before assigned to transport machineries. The protein family, small GTPases, establish membrane identity on various organelles and vesicles. They act as the molecular switches and once activated, they are attached to the membrane and recruit the same molecular to the surrounding membranes. To quantitatively understand this complicated process in which diffusion plays a key role, we utilise synthetic model systems to dissect how individual reaction affects the overall kinetics and dynamics.
  2. Evolution of switching rate between cell fates. During evolution, positive feedback often emerges in gene regulation and leads to a switch like response that allows activating certain genes only when the environmental stimuli reach a certain threshold. However, such feedback systems can also result in a phenomenon called cellular memory, or hysteresis. In this case, the cellular response to an environmental stimulus depends on whether the cell has been activated before: a previously activated cell stays activated and vice versa. Obviously, cellular memory slows down or even prevents proper response, which can cause adaptation disadvantage. We synthesise gene circuits that reflect such conditions to study how such switching rates affect fitness and how switching rates evolve in a population under rapid and extreme environmental changes.

 

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Enquiries: Phone: +44 (0)1227 823743

School of Biosciences, University of Kent, Canterbury, Kent, CT2 7NJ

Last Updated: 18/05/2017