Vakoc is now exploring how mutations that increase the activity of MLL in leukemia affects the pattern of reactivation of the gene into the cells again and how it could contribute to abnormal cell proliferation and differentiation seen in leukemia. Now we have a clearer picture of what MLL normally in healthy cells to help gene expression information to travel from the mother cell to daughter cells, said Vakoc. These results may help to understand how mutated MLL subverts inheritance mechanisms in leukemic cells.

Scientists say that the newly formed cells inherit the knowledge of which genes need to become very active at this time with a useful protein bookmarks of these genes during cell division of the mother. Their findings appear in the December issue of Molecular Cell 24 of

During cell division or mitosis refers to any activity of the gene is temporarily closed. The cell divides chromosomes – the X-shaped coils of DNA – condense into tight clumps and expel most of the proteins that attach to DNA to maintain gene expression.

Vakoc The team was surprised to find, however, that unlike other chromosome-related molecules, the MLL protein remains attached to the chromosomes during mitosis. The genome surveys that compared MLL chromosomal binding sites before and during division – a comparison of the first of its kind – has revealed a touch of the second.

The bookmarking protein, called mixed lineage leukemia MLL, is known to trigger when the gene that encodes it becomes mutated. MLL mutations are among the most common genetic aberrations in leukemia, occurring in approximately 10 percent of cases of leukemia.

In the search and bookmark this group of genes highly expressed in the division, MLL post-mitotic kick that helps turn genes back, said Vakoc. In support of this idea, his team found that when MLL was depleted, the reactivation of these genes was delayed and have launched the slowest. Cling to these genes, MLL provides a beacon to which other proteins can home, that the revival of activity of the gene.

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Leukemia-related protein highly active ‘Bookmarks’ genes during cell division