As noted above, transgenes frequently become silenced in germ cells, and that silencing becomes essentially permanent in all subsequent generations.
The trade-off is that some effectors may become inadvertently silenced through proximity to silenced neighboring TEs, or through becoming overly duplicated.
Furthermore, TSG may become epigenetically silenced by hypermethylation of CpG islands located in their promoter regions, which are usually unmethylated in normal tissue [ 2, 3].
Diploidization allows that one gene could retain its original function whereas the other copy may become epigenetically silenced or inactivated by mutations.
A Cornell-led team has discovered that at the onset of a rare liver disease, a small non-coding RNA molecule becomes silenced, a finding that may hold the key to treatment.
The induced expression of endogenous Oct4, Sox2, (and partially of c-myc) homologs in all species and their continued expression when the mouse transgenes became silenced suggests that these genes may be playing more conserved inductive roles.
Cells may become so transcriptionally inactive that p16 itself, although initially expressed, becomes silenced in some cells, growth stasis being maintained by silencing of genes required for cell proliferation.
If transgene silencing is transcription-dependent, then the nature of the promoter and enhancer elements in transgenes may also have a large bearing on whether or not a transgene becomes silenced.
Second, one copy of a duplicate gene pair may retain the original function, but the other copy may become lost or silenced [ 3, 13, 14, 23- 26].
