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About Teresita

My research interests are focused on the biological roles of transition metals, such as Cu+, Zn2+, Co2+, and Mn2+, in the development of mammalian cells. Transition metals are micronutrients that are required as co-factors in metalloenzymes. High levels of transition metals are a potential hazard to the cells due to their chemical reactivity. As a postdoctoral fellow, I investigated the biological, biochemical, and mechanistic details of metal transport (entry-exit) and buffering systems. I described for the first time the mechanism for copper (Cu) export by Cu+-ATPases (CopA) in bacteria. Cu is chelated in the cells by cytosolic (CopZ) and periplasmic/extracellular (CusF) chaperones. I established the fine mechanism of Cu delivery from CopZ to CopA and from CopA to CusF and showed how mutation of these proteins impairs the transport system. I demonstrated the importance of specific protein-protein interactions to allow the transfer between Cu chaperones and the transporters. I also demonstrated the importance of different transition metals in the survival of pathogens such as Mycobacterium tuberculosis and Pseudomonas aeruginosa. My ultimate goal is to understand the role of transition metals in mammalian cell differentiation and development. Therefore, I pursued a second postdoctoral stay to expand my knowledge in the differentiation of mammalian cells. I worked with primary myoblasts derived from mouse satellite cells to study the SWI/SNF ATP-dependent chromatin remodeling enzymes, in particular the role of phosphorylation-dephosphorylation of the catalytic subunit Brg1, and how this affects myogenesis. I described novel signal transduction mechanisms that modify the activities of SWI/SNF chromatin remodeling enzymes via post-translational modifications of the ATPase subunits.

As an independent researcher, I utilize a multidisciplinary approach to elucidate fundamental questions of the biology and biochemistry of transition metals, in particular Cu, to cell differentiation and developmental models. I use cultured primary myoblasts derived from mouse satellite cells as a model, as this system has an intrinsic high demand of Cu for mitochondrial energy production and maintenance of redox homeostasis. Preliminary studies from my lab show that Cu is required for myogenesis, as cytoplasmic fluxes of this ion have been detected; moreover, myoblasts depleted of Cu fail to differentiate. We hypothesize that Cu can follow different pathways to enable myogenesis, from transcriptional regulation, cell signaling, metallation of lineage specific cuproenzymes to mitochondrial biogenesis. We are particularly interested in investigating the molecular mechanisms by which Cu may contribute to myogenesis. These novel basic science discoveries can be extremely important to health and disease/translational medicine. I aim to understand the effect of aberrant Cu homeostasis and its effect on muscle deficiencies associated with diseases such as Menkes’, Wilson’s, and fatal Cu-dependent mitochondrial myopathies. During my career, I have aimed to define basic mechanisms of the transport and cell biology of different transition metals in pathogens. Now, I hope to contribute to the fundamental mechanisms related to Cu transport and advance our knowledge from basic to translatable research by identifying molecules and novel mechanisms that might be potential targets for therapies.