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However, induction of ectopic polar body by a fertilizing sperm chromatin poses a risk of paternal genome loss, as we have shown that sperm chromatin has a high frequency of being extruded with the ectopic polar body.
In contrast to the frequent KSHV genome loss observed from Kaposi's Sarcoma spindle cells [51], MuHV-4 episomes were maintained in transformed fibroblasts for at least 3 weeks without evidence of viral lytic gene expression.
In summary, post-meiotic remodeling and repackaging of sperm chromatin may play a previously unappreciated role in orchestrating cytoskeletal assembly but limiting its ability to induce spindle formation during fertilization, thus constituting a protective mechanism to prevent ectopic polar body extrusion and a potential of paternal genome loss during fertilization.
The usually observed cone formation instead of ectopic polar body extrusion induced by sperm chromatin during fertilization is due to special sperm chromatin compaction which restrains it from rapid spindle induction and therefore provides a protective mechanism to prevent a possible paternal genome loss during ectopic polar body extrusion.
It recently was hypothesized that PSR could induce paternal genome loss by altering histone modification in the developing N. vitripennis spermatids (Swim et al. 2012).
These genes encode for a group of proteins that guard the fidelity of the genome; loss of function on any of these genes can result in carcinogenesis.
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It has been reported that the importance of a gene is negatively correlated with its evolutionary rate [28], and as guardians of the genome, loss-function of tumor suppressors may be more critical in tumorigenesis, as demonstrated by Cui et al. [29].
For example, the Drosophila melanogaster genome losses less than a single base pair per generation [ 47].
These genome losses were not seen in any of 31 CP, 6 accelerated and 12 BCM samples or controls.
Either they represent genome losses associated with cross lineage rearrangements known to occur in both ALL and AML, or they represent a bona fide event with oncogenic potential.
The FISH results obtained in five cases, for which chromosome preparations were available, are summarized in Figure 5. Genome losses were confirmed in all cases studied as illustrated by the results for case 164.
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