Sunday September 23, 2012 11:30 - 11:45 @ Rhodes 6 

Troponin I loss yields to cell polarity loss, cell cycle arrest and cell competition

Abstract:

Troponin I (TnI) is an actin binding protein involved in muscle contraction but has a novel non-muscular function recently documented. The underlying mechanisms and relevance of this new role of TnI are under study. TnI is expressed in the preblastodermic embryo, prior to muscle cell formation or their precursors exist. TnI is accumulated in the cytoplasm of the cell, and translocated to the nucleus during mitosis. TnI mutations generate chromosomic aberrations lethal for the cell.

TnI is accumulated apically in epithelial and secretory cells in salivary glands. Lack of TnI causes DNA disorganization and polarity defects in the salivary gland disrupting the formation of the sac. In TnI mutants polarity proteins such as Disc-large (Dlg) or Pins are mislocalized in the epithelium, altering the apico basal polarity of the cell. Aditionally, TnI loss in epithelial cells induces a lower proliferation rate and the elimination of the cells through apoptosis and cell competition mechanisms. Moreover, in neuroblasts, the asymmetric division needs polarization of the mother cell and the reduction of TnI in neuroblasts induce a lower rate of division. Together, all these evidences indicate a role for TnI in the maintenance of the apico-basal polarity in cells. We are currently studying if TnI interacts directly with cell polarity proteins and how TnI might be use as a cargo to deliver certain proteins to their correct localization. Candidate proteins as Scribbled, Lgl or Dlg with protein-protein interaction PDZ domains also present in TnI are under study, opening the possibility of a direct interaction of Tn I with the machinery sustaining apico basal polarity.

TnI mutants display early phenotypes suggesting non-muscular functions of the protein. TnI plays a key role in the organization of the DNA and cell polarity in epithelium, neuroblasts and salivary glands. TnI mutant cells are suboptimal and eliminated during development by cell competition.