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Hence, the inverse age- d N / d S relationship in mouse duplicates suggests less effect of genetic buffering in ancient duplicates than that in recent duplicates, implying that the genetic buffering of duplicates g could be age dependent.
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Shiu et al. (2006) examined similar lineage-specific patterns when comparing human and mouse duplicates, suggesting that the larger population size and shorter generation interval in murine species could account for more effective natural selection and retention of duplicated genes.
Our results suggest that duplication age and genetic buffering determine the essentiality of mouse duplicates.
In fact, (1) suggests that three parameters, t (duplication age), g (genetic buffering), and λ (loss rate of functional compensation), together determine the gene essentiality of mouse duplicates.
To be clear, we used P E -dup(t) for the age-bin (t) of mouse duplicates.
In contrast, 58.9% of the mouse duplicates were created 500 mya (unpublished data).
Similar expression patterns may suggest redundancy among the duplicated genes and divergence of the expression patterns of duplicated genes suggests a non-redundant function.
However, early research in mice suggests that exercise can help prevent this slowdown.
Since most of the mouse WGD duplicates are ancient duplicate genes, their conclusion that the mouse knockout duplicate puzzle may be caused by sampling bias of WGD duplicate genes is consistent with age-distribution hypothesis.
Meanwhile healthy tissues are spared, tests in mice suggest.
A sporadic distribution of duplicated genes could suggest ancestral duplications and multiple losses or independent origins of duplicated gene.
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