In addition to this, recent experiments suggest that the content of lamin B-negative micronuclei is not replicated during the entire cell cycle, suggesting the dilution of micronuclear content during cell proliferation. Taken together,it appearsthat the content of micronuclei may be eliminated from the cells by several different, separable mechanisms. The genetic material was neither transcribed nor replicated in the Pristinamycin lamin-less micronuclei. Therefore, the question of why and how the structural heterogeneity of micronuclei arose has important implications. We show here that part of the reason derives from the mechanism of micronuclei generation, as most of the chromatin bridge-derived micronuclei had condensed chromatin that was not associated with lamin B, whereas the lagging chromatid-derived micronuclei had more relaxed chromatin with lamin B. The question of why and how these differences arise between micronuclei is important because the answer will contribute towards an understanding of how the nucleus is reconstructed after the completion of mitosis. Our future studies will address this question. LY2409881 telomeres are DNA-protein complexes comprised of repetitive non-coding DNA sequences at the ends of eukaryotic chromosomes and the proteins that bind these sequences. In mammals, telomeres consist primarily of TTAGGG sequences. Telomeres prevent chromosome erosion and loss of coding sequences due to the end-replication problem. Loss of telomeric DNA is linked with cellular senescence and aging, and likely resembles double-strand breaks that activate DNA damage response pathways. While cell growth continuously reduces telomere length, cancer cells become immortalized by activating mechanisms of telomere maintenance. The most common mechanism is expression of the enzyme telomerase, which catalyzes the addition of repeats to maintain telomere length. Approximately 15% of human tumors maintain telomeres independently of telomerase and use a recombination-based mechanism known as alternative lengthening of telomeres to maintain telomere lengths.