TREACLE DEPLETION IN Danio rerio INDUCES OXIDATIVE STRESS AND APOPTOSIS

MOUGUELAR, V; PORCEL DE PERALTA, M; COUX, G; CALCATERRA NB

Rosario

Congreso; L reunion de SAIB; 2014

SAIB

Treacher-Collins Syndrome (TCS) is a disorder of craniofacial development due to mutations in TCOF1, which encodes the protein Treacle. TCS patients show variable expressivity in phenotype. Treacle deficit seems to increase cranial neural crest cells apoptosis. Recently, it has been informed that Treacle has antioxidant activity in pneumocytes. We developed a TCS-like model injecting in zebrafish embryos morpholinos against the tcof1 ortholog (TcofMO). The aims here were to assess in TCS-like zebrafish embryos: I) the apoptosis occurrence (pattern and gene markers) and, II) the oxidative stress induction. We studied noxa, cyclinG1, trp53inp, and hsp70 expression by RT-qPCR; the levels of reactive oxygen species (ROS) by incubation with DA-DCFH; and apoptosis events by Acridine Orange stain. The expression of apoptotic marker genes was induced in TCS-like embryos (noxa 3.0±0.4, cyclinG1: 3.5±1.0 and, trp53inp1: 1.4±0.1 times vs. control morpholinos (MisMO) embryos). Besides, TCS-like embryos showed increased hsp70 expression (2.0±0.6 times) and ROS levels (MisMO=46.6±1.2 andTcofMO=69.8±2.5 UA, p