When chromosome cohesion goes wrong

SCAN Seminar

Title: When chromosome cohesion goes wrong

Speaker: José António Melo da Costa Nunes

Afilliation: Disease and Stress Biology

Abstrat:

During the mitotic cell cycle, sister chromatids are kept bound together (cohese) after DNA replication, until the onset of mitosis. When mitosis takes place, sister chromatids segregate to opposite poles of the cell giving origin to daughter cells containing the same set of genetic information. Lack of functional chromosome cohesion in mitosis (as well as in meiosis) leads to chromosome mis-segregation, giving origin to aneuploidy and hence genetic disorders such as Down syndrome and XYY syndrome. Ultimately, chromosome mis-segregation can lead to daughter cell death.
RAD21 is one of the key proteins involved in chromosome cohesion. This protein is required not only for a correct mitotic chromosome segregation, but also for the repair of DNA double strand breaks (dsb). Its role in DNA dsb repair has been attributed to its function in keeping sister chromatids in close vicinity, to allow homologous recombination mediated DNA repair. Lack or faulty repair of DNA dsb can lead to the formation of chromosome fragmentation, InDel(s), translocations, etc. 
While in many model organisms there is only one RAD21 gene, in Arabidopsis there are three RAD21 homologues, one of which (AtRAD21.1) is the only one responsive to DNA dsb damage inducing agents. Accordingly, atrad21.1 mutation does render plants more sensitive to ionising radiation induced DNA dsb damage.  
During meiosis, tightly regulated chromosome segregation also takes place, as well as programmed induction and repair of DNA dsb (recombination), making it a good system to identify new genes required for accurate chromosome segregation and DNA dsb repair.

I shall be presenting some data obtained from a meiotic mutant screen carried out with the goal of identifying novel chromosome segregation mutants as well as on the characterisation of the RAD21 Arabidopsis cohesins, focusing mostly on the DNA dsb repair role (PTDC/BIA-BCM/64192/2006).

Brief C.V.
  DPhil at the University of Oxford, UK
  Previous Post-Docs:
         University of Oxford, UK; Universität Zürich, CH; Universidade Técnica de Lisboa, PT
  Current Post-Doc:
          Disease and Stress Biology lab.- ITQB, Universidade Nova de Lisboa, PT