Abstract
Centrosomes are the major microtubule organizing structures in vertebrate cells. They localize in close proximity to the nucleus for the duration of interphase and play major roles in numerous cell functions. Consequently, any deficiency in centrosome function or number may lead to genetic instability. Several viruses including retroviruses such as, Foamy Virus, HIV-1, JSRV, M-PMV and HTLV-1 have been shown to hamper centrosome functions for their own profit, but the outcomes are very different. Foamy viruses, HIV-1, JSRV, M-PMV and HTLV-1 use the cellular machinery to traffic towards the centrosome during early and/or late stages of the infection. In addition HIV-1 Vpr protein alters the cell-cycle regulation by hijacking centrosome functions. Enthrallingly, HTLV-1 Tax expression also targets the functions of the centrosome, and this event is correlated with centrosome amplification, aneuploidy and transformation.
Highlights
Centrosomes are animal-specific non-membranous organelles that localize in close proximity to the cell nucleus for the duration of interphase. Their structure is highly conserved among higher eukaryotes. It usually consists of a pair of centrioles joined by fibers connecting their proximal ends which are embedded into a proteindense matrix called the pericentriolar material (PCM) [2,3]
The PCM is an ordered lattice that anchors a large number of microtubule (MT)-associated proteins, many of which bear putative coiled-coil domains, a tertiary structure known to facilitate protein-protein interactions
Centrioles play a role in the organization of the microtubular cytoskeleton, but they do not make direct contact with the MTs which nucleate from the γ-tubulin ring complexes located within the PCM
Summary
Besides an indirect role of Tax via cell-cycle regulation alterations, the viral protein could be directly implicated in aneuploidy and centrosome amplification. If this was the case, a fraction of Tax should be located close the centrosome in order to induce centrosome multiplication (Figure 4). Proposed that the ability of Tax to bind RanBP1 (one of the major cytoplasmic effector of Ran) is a critical event for targeting the viral protein to the centrosome (Figure 5) This interaction is necessary but not sufficient for inducing aneuploidy [87].
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