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Chemoresistance in cancer has previously been attributed to gene mutations or deficiencies.
RTT has mostly been attributed to gene deregulation caused by a lack of MeCP2 expression in adult neurons (Luikenhuis et al., 2004).
Similar discrepancies between noncoding- and coding-sequence trees in several organisms have been attributed to gene conversion processes that have a greater effect on coding sequences [ 63].
Low expression of exogenously introduced constructs in Chlamydomonas is a well-known phenomenon, which has been attributed to gene silencing [ 18].
It remains unclear why Brassica species have the capacity to generate such a wide range of morphological forms, although this has been attributed to gene duplication, intergenomic heterozygosity and epigenetic phenomenon [ 37- 39].
Long operons of identical or nearly identical units of rRNA genes are very common in eukaryotic genomes, and the high level of similarity among the copies has been attributed to gene conversion and other mechanisms that result in concerted evolution [ 63].
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Could these alternatively be attributed to gene flow from a more archaic population that survived alongside modern humans?
These differences could be attributed to gene variability [ 152].
The absence of this AFP within the genomes of intervening species was attributed to gene loss.
Around 5% of breast cancers can be attributed to gene mutations.
This difference can be attributed to gene PET9 (the ninth gene from the top in Fig. 3c).
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