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Developmental Biology Program   Member Publications
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Prof William Chia, Temasek Senior Investigator

Bill Chia was educated at the California Institute of Technology where he graduated with honors in Biology (1973). He received his Masters degree in Molecular Biology from the University of Wisconsin at Madison (1976) and PhD in Biochemistry from Imperial College, University of London (1980). After 3 years of postdoctoral training as a MRC Fellow in the Department of Genetics in Cambridge University he became a faculty member in the Biochemistry Department at the University of Bristol Medical School. He came to Singapore for the first time at the beginning of 1990 to join the Institute of Molecular and Cell Biology where he became Professor and Deputy Director for Academic Affairs. He returned to the MRC Centre for Developmental Neurobiology at King’s College London as Professor of Developmental Genetics and Wellcome Trust Principal Research Fellow in 2001. He has been the Executive Director of Temasek Life Sciences Laboratory since 2004.

You may wish to contact Prof William CHIA at:
Tel: (65) 6872 7000, 6872 7554 (DID) or 6872 2227 (lab) Email: wchia@tll.org.sg


For information on PhD studies at TLL, click HERE


Research Interests
  • Neural development
  • Asymmetric cell division
  • Myoblast fusion

Research Projects

My group is trying to understand how cell fates are specified - how neuronal diversity in particular and cellular diversity in general are generated - during development using Drosophila as a model. Asymmetric cell division is a mechanism by which distinct sibling cell fates can be specified. For neural progenitor cell divisions, distinct daughter fates are specified, in part, through protein and RNA determinants (e.g., Numb and Prospero) which are asymmetrically localised to the basal cell cortex during mitosis; following progenitor cell division, they are preferentially inherited by just one of the daughters. These cell fate determinants act to make the cell which inherit them different from its sibling. We are currently elucidating the mechanisms underlying how a complex of apically localised proteins comprising of two evolutionarily conserved signaling cassettes, the Par protein cassette and a heterotrimeric G protein related protein cassette, linked together by the protein Inscuteable, act to mediate and coordinate key features of the neural progenitor asymmetric division which include: 1) basal localisation of cell fate determinants, 2) apicobasal orientation of the mitotic spindle and 3) the generation of an asymmetric apically biased spindle leading to the generation of daughters of unequal sizes. We are currently taking two approaches to discover novel genes involved in asymmetric divisions. The first approach is a large scale clonal screen in which mutant tissues are generated several days prior to the assessment for loss of neuroblast polarity in the post-embryonic central nervous system. A second approach has been based on looking for molecules which are asymmetrically localised since the majority of key player which regulate asymmetric divisions are themselves asymmetrically localised. Using these approaches, we hope to overcome the limitations imposed by the fact that the majority of genes have maternal components which can potentially mask the effects of the loss of zygotic function during embryonic development, and further understand the process. In addition to asymmetric division related issues, we are also interested in problems relating to how neuroblasts, myoblasts and the neuroectoderm are specified and how somatic muscles are formed.

 

 
 
   
   
   
   
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