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The inactivation of any of at least five of the six MCM subunits during S phase quickly blocks ongoing elongation. As a critical mechanism to ensure only a single round of DNA replication, the loading of additional MCM2-7 complexes into pre-RCs is inactivated by redundant means after passage into S phase. [26]
In this case, the redundant part of the gene remains in the genome due to the proximity to the area that codes for the unique function. [17] The reason redundant genes remain in the genome is an ongoing question and gene redundancy is being studied by researchers everywhere. There are many hypotheses in addition to the backup and piggyback models.
How nature sets the disproportionate numbers of particles remain unclear, but can be found using the theory of diffusion. One example is the number of neurotransmitters around 2000 to 3000 released during synaptic transmission, that are set to compensate the low copy number of receptors, so the probability of activation is restored to one. [19 ...
Duplication creates genetic redundancy, where the second copy of the gene is often free from selective pressure—that is, mutations of it have no deleterious effects to its host organism. If one copy of a gene experiences a mutation that affects its original function, the second copy can serve as a 'spare part' and continue to function correctly.
Degenerate components compensate for one another under conditions where they are functionally redundant, thus providing robustness against component or pathway failure. Because degenerate components are somewhat different, they tend to harbor unique sensitivities so that a targeted attack such as a specific inhibitor is less likely to present a ...
ADP-ribose. ADP-ribosylation is the addition of one or more ADP-ribose moieties to a protein. [1] [2] It is a reversible post-translational modification that is involved in many cellular processes, including cell signaling, DNA repair, gene regulation and apoptosis.
Although a now-classic series of experiments by Schaper [3] in the late 1960s and '70s expanded our understanding of the mechanisms by which these usually redundant, microscopic (40-10 um in diameter in their native state) ur-arterioles are transformed by ischemia or stenosis into vessels with life-preserving blood capacity, [4] equally as many ...
However silencing of redundant genes occurs rapidly in new polyploids through genetic and epigenetic means. This primarily occurs because redundancy allows one of the two genes present for each locus to be silenced without affecting the phenotype of the organism, and thus mutations that eliminate gene expression are much less likely to be ...