Our cells ask a lot of our chromosomes. Chromosomes contain all of our genetic material, but are required to compact themselves into skinny little things that can be easily divided during cell division. Throw a terrible virus into the mix, and chromosomes start to have trouble with their duties. During mitosis, duplicated chromosomes separate after receiving a signal allowing anaphase to begin. Until this signal is relayed, each pair of chromatids stays attached to one another by the cohesin protein complex. Premature chromatid separation was recently found in some types of white blood cells in HIV-infected people, and can lead to cells having an incorrect number of chromosomes. This same research group more recently showed that this HIV-induced premature chromatid separation is caused by Vpr, an HIV accessory protein. Vpr causes premature chromatid separation by disrupting the higher-order structure of DNA surrounding the centromere, the region where kinetochores allow attachment to the mitotic spindle. In the images above, the cohesin complex (pink, arrows) is found within the centromere of a control chromatid pair (left). In cells expressing the HIV accessory protein Vpr (right), the cohesin complex is absent from the centromere of a loosely-bound chromatid pair (arrowheads).
Shimura, M., Toyoda, Y., Iijima, K., Kinomoto, M., Tokunaga, K., Yoda, K., Yanagida, M., Sata, T., & Ishizaka, Y. (2011). Epigenetic displacement of HP1 from heterochromatin by HIV-1 Vpr causes premature sister chromatid separation originally published in The Journal of Cell Biology, 194 (5), 721-735 DOI: 10.1083/jcb.201010118
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