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mcbucs@
imcb.nus.edu.sg

Tel: (65)6874 3518
Lab: (65)6874 6680

 
 
   

Assoc Professor Uttam . C . Surana

Academic Qualifications
Ph.D. 1986 University of Arizona


Born in India, Uttam Surana undertook his graduate studies at the University of Arizona and obtained a PhD from the Dept. of Molecular and Cellular Biology in 1986. Thereafter, he moved to the Dept. of Engineering at the University of Cambridge and spent 2 years studying the mechanical properties of bacterial cell surface polymers and their role in cell shape determination. He spent the subsequent four years as a postdoctoral fellow at the Institute of Molecular Pathology in Vienna investigating various aspects of cell division in the budding yeast. He joined the IMCB in 1992 and is now an Associate Professor.

 

Research Interests
  1. Cell Cycle Regulation In The Budding Yeast S. cerevisiae

    ...Of Destruction, Division and Daughters

    It is through cell division that living cells make more of themselves and organisms become multi-cellular during their development. Cellular activities leading to division are highly regulated both in time and space. Any violation of this precision can lead to genomic instability resulting in either unbridled proliferation (cancerous growth) or death of parent and progeny cells.


Budding yeast cells showing localization of a bud-site component

Valuable insights into the way cell division is controlled in complex systems, such as human cells, have come from investigations of relatively simple eukaryotes. The budding yeast Saccharomyces cerevisiae is one such test organism that has served remarkably well because of its amenability to genetic manipulations. The sequencing of the entire S. cerevisiae genome has now added a new dimension to its usefulness as an experimental system. A budding yeast mother has very strict priorities. For example, it will not depart from mitosis until it has properly segregated their chromosomes into the daughter. Also, it neither initiates separation from its old daughter (cytokinesis) nor begins forming a new daughter until it exits mitosis. The Surana Lab has focused their investigations on mechanisms that ensure a precise coordination of these events during a normal division cycle. Over the last few years it has become clear that the ubiquitin-mediated proteolytic destruction of mitotic regulators is central to the coordination of mitotic events. A multi-subunit protein complex called the Anaphase-promoting complex (APC) is the agent that catalyzes the destruction event facilitating both chromosome segregation and the final departure from mitosis. Through genetic and biochemical analyses, this lab has identified Cdc20 as an essential activator of the APC. Further studies on Cdc20 have uncovered a mechanism whereby Cdc20, together with its homologue Hct1, mediates the inactivation of the mitotic kinase Cdc28-Clb via proteolytic destruction of Clb proteins, ensuring a rapid but timely exit from mitosis.Lab members have also explored the regulatory links between the inactivation of the Cdc28-Clb kinase and the construction of a new daughter. Their studies reveal that mitotic kinase is a potent inhibitor of daughter formation; it prevents a mother from assembling the site at the cortex from where a new daughter is to emerge. These findings provide a cellular logic to the mitotic kinase inactivation, which invariably precedes the emergence of a new daughter. Thus, by studying the coordination of various cellular events, Dr. Surana and his colleagues hope to understand the molecular circuits through which eukaryotic cells exercise temporal and spatial control over their activities during cell division. In addition to providing clues to the organizing principles of living cells, such efforts may also lead to the identification of key regulators that could serve as targets for the therapeutic interventions against growth of cancerous cells.

 

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