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Background: Aneuploidy is widely observed in both unicellular and multicellular eukaryotes, usually associated with adaptation to stress conditions. Chromosomal duplication stability is a tradeoff between the fitness cost of having unbalanced gene copies and the potential fitness gained from increased dosage of specific advantageous genes. Trypanos...
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(See also the 8 PDF files appended below) This work is based on a hypothesis I formulated in 2006 pertaining to targeting particular aspects of microtubule dynamics for cancer treatment. Thereafter, my goal was to investigate breast cancer-specific aberrations at the cellular level. The microtubules are essential polymer filaments composed of tubul...
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... Genomic plasticity, which can include entire chromosomes or gene deletion/duplication, is an important tool in response to environmental changes like the ones faced by parasites. Aneuploidy, which refers to an unequal number of chromosomal copies, is an ancestral characteristic in trypanosomatids being present in several species of this family, including Leishmania spp., T. cruzi, and the basal Paratrypanosoma confusum [16]. However, aneuploidy later evolved to be almost absent in T. brucei and closely related species (T. ...
... However, aneuploidy later evolved to be almost absent in T. brucei and closely related species (T. congolense and T. vivax) [16]. The peculiarities of T. brucei genomic organization may have contributed to this loss, since this parasite presents a larger chromosome size, and hence an increased fitness cost of aneuploidy (i.e., a higher number of genes per chromosome leads to an increased number of genes in an unbalanced proportion). ...
... The exceptions are the genes related to the ancestral chromosomal duplication (named Duplicated31) containing housekeeping genes that were also maintained in T. brucei. It is interesting to note in this parasite and T. cruzi, the Duplicated31 is enriched in genes involved in glycosylation and surface-protein anchoring, i.e., during evolution these parasites transferred to Duplicated31 genes that are crucial for host-pathogen interaction, since both parasites require GPI-anchored proteins for cellular invasion and immune evasion [16]. ...
The neglected Chagas disease (CD) is caused by the protozoan parasite Trypanosoma cruzi. Despite CD dispersion throughout the world, it prevails in tropical areas affecting mainly poor communities, causing devastating health, social and economic consequences. Clinically, CD is marked by a mildly symptomatic acute phase, and a chronic phase characterized by cardiac and/or digestive complications. Current treatment for CD relies on medications with strong side effects and reduced effectiveness. The complex interaction between the parasite and the host outlines the etiology and progression of CD. The unique characteristics and high adaptability of T. cruzi, its mechanisms of persistence, and evasion of the immune system seem to influence the course of the disease. Despite the efforts to uncover the pathology of CD, there are many gaps in understanding how it is established and reaches chronicity. Also, the lack of effective treatments and protective vaccines constitute challenges for public health. Here, we explain the background in which CD is established, from the peculiarities of T. cruzi molecular biology to the development of the host’s immune response leading to the pathophysiology of CD. We also discuss the state of the art of treatments for CD and current challenges in basic and applied science.
