Our set of examples adds evidence for the importance of duplication mechanisms of genetic material for the generation of non-coding RNAs and gives a plausible explanation for the generation of relatively large complementary transcripts like trans-NATs.
Our results do not imply a functional relation of the trans-NAT arising from pseudogenes over their respective parental genes but add evidence for it and stress the importance of duplication mechanisms of genetic material in the generation of non-coding RNAs.
Little is known about the nature of the biological mechanisms underpinning handedness/cerebral lateralization (although McManus 24, 43 speculated that it may have involved duplication and modification of mechanisms originally responsible for situs lateralization).
None of these three patterns was confined to a particular plant group (algae, lower plants, eudicots and monocots), implying that the relative importance of duplication mechanisms, like other traits of FBX loci, differed among the plant lineages.
While this similarity might be the result of convergent evolution due to the availability of duplication mechanisms and processing enzymes in the cell, it might also stem from evolution from a common ancestral RNA molecule or evolution from one small RNA type to the other.
Given the intensive experimental control required to assess human physiological period, our laboratories have taken advantage of the duplication of the molecular mechanism of the circadian clock in most mammalian tissues to measure period length in human fibroblasts.
Gene duplications occur by a variety of mechanisms ranging from local tandem duplication of individual genes to global duplication of entire genomes.
A future opportunity is in examination of large gene family databases like Ensembl [ 60], HOGENOM [ 61], or TAED [ 62], a mixture model of duplicate processes can be applied across all gene families and duplication events to enable a posteriori probabilistic identification of duplication retention mechanisms for individual gene duplication events.
Together, these results suggest a very accurate mechanism of repair in coding regions, a mechanism for duplication of sequences, and a less accurate mechanism of repair in noncoding sequences.
By identifying alignments that cross intron-exon boundaries we were able to distinguish between retrotransposition and unequal crossing over as (duplication) mechanisms of origin of LSGs in the Arabidopsis thaliana genome.
