An alternative to the selfish DNA hypothesis is that adaptive mutations play a vital role in the persistence of ISs [ 4, 18, 19].
One might assume that genetic mutations in such a vital structure would be disastrous, and in humans, mutations in the best-known, textbook enzyme at the heart of the pre-initiation complex — the massive enzyme called RNA polymerase II — are very likely to be lethal before birth.
As reported in the recent exome sequencing of CHD, de novo mutations in chromatin markers played a vital role in regulating cardiac development genes [ 36].
Among the various diseases causing mutations, single nucleotide polymorphisms (SNPs) play a vital role in defining individual's susceptibility to disease and drug response.
For instance, the mutations of APC, KRAS, and TP53 play a vital role in the evolution of colorectal cancer [ 4].
Another 12,000 people suffer from hemophilia A, the result of mutations in the gene for Factor VIII, also a vital component of the body's blood-clotting system.
In addition to mutations in targeted oncogenes, signaling cross-talks among pathways play a vital role in such drug inefficacy.
Homozygosity mapping has played a vital role in the identification of many recessive causal mutations.
Constant proliferation is a vital feature of stem cells, and in gastrointestinal tissues mutations are likely to result in expansion of altered stem cells, increasing the probability of additional mutations and tumor progression [ 12].
The core Mediator complex is a vital component of eukaryotic transcription [72], potentially explaining why relatively few human mutations have been identified.
