Dr Jun-yong Huang
Lecturer

  • Email: junyong.huang@ncl.ac.uk
  • Telephone: +44 (0) 191 208 5480
  • Fax: +44 (0) 191 208 5296 (lab)
  • Address: Institute for Cell and Molecular Biosciences
    The Medical School
    University of Newcastle
    Framlington Place
    Newcastle
    NE2 4HH
    UK

Roles and Responsibilities

Institute laser safety supervisor
School recruitment committee member

Qualifications

PhD

Memberships

The Genetics Society
British Society for Developmental Biology
British Society for Cell Biology

Undergraduate Teaching

BGM1003 pratical and seminars.

BGM3047- Integrated Biochemistry and Genetics

CMB3000-Undergraduate Research Project supervision 

Postgraduate Teaching

MMB8008 MRes module teaching, module leader

Research Interests

Cell cycle control
Confocal and Fluorescence imaging
Drosophila genetics and developmental biology

Other Expertise

Drosophila Genetics, molecular biology and biochemistry

Current Work

Faulty cell division leads to aneuploidy and genetic instabilities that contribute to the progression of cancers and many other diseases including birth defects and Alzheimer's. To prevent this from happening, cells have evolved a mitotic surveillance mechanism, the spindle assembly checkpoint (SAC), to ensure a mother cell segregates its duplicated genomes equally into its two daughter cells with high fidelity during mitosis. Many important proteins involved in this process have been identified, but exactly how they relay signals to coordinate the faithful mitotic progression still remain to be answered. This lab uses biochemical, genetic, transgenic and microscopic methods to tackle these problems in Drosophila melanogaster (the fruit fly). Drosophila is an extremely tractable experimental system, a much simpler and better-understood organism compared to the human but shares fundamental processes in common. The SAC mechanism involves the proteins Mad2, BubR1 and Cdc20. Mad2 and BubR1 are inhibitors of the APC/C, an E3 ubiquitin ligase, while Cdc20 is an activator. Once activated, SAC can inactivate the APC/C to prevent destruction of two major mitotic regulators, Cyclin B and Securin, thus delaying the sister chromatid segregation. We have shown that the destruction of the Cyclin B is spatial-temporal regulated and that two APC/C core subunits, Cdc27 and Cdc16 are not always colocalised within cells. Cdc27 associates with mitotic chromosomes, but Cdc16 does not. This raises an intriguing possibility, that the activity of the mitotic APC/C is also spatial- temporally regulated. We also show that the SAC component BubR1, but not Mad2, is required for Cdc20 kinetochore recruitment. This provides an important new insight into the SAC mechanism. The functional interactions between the SAC mechanism and the apoptosis pathway are also under investigation.

Research Roles

Principal investigator.

Funding

Wellcome Trust Project Grant:RES/0120/7244
Wellcome Trust Project Grant:RES/0120/7360
BBSRC equivalent, Faculty funded PhD studentship.
BBSRC DTA PhD studentship.