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Published on: December 28, 2015
Molecular evolution of the HBII-52 snoRNA cluster
Satu Nahkuri1, Ryan J Taft, Darren J Korbie
1Institute for Molecular Bioscience, University of Queensland, St. Lucia, Queensland 4072, Australia.
The HBII-52 snoRNA, linked to Prader-Willi syndrome, shares evolutionary origins with SNORD119. Analysis of mammalian genomes reveals their common ancestry and potential roles in serotonin receptor regulation.
Area of Science:
- Genomics
- Molecular Biology
- Evolutionary Biology
Background:
- HBII-52 is a human brain-specific C/D box small nucleolar RNA (snoRNA) potentially regulating serotonin receptor editing and splicing.
- Multiple copies of the HBII-52 gene are located in an imprinted locus associated with Prader-Willi syndrome, downstream of the SNRPN gene.
- The SNRPB gene, a precursor to SNRPN, expresses the snoRNA SNORD119 from its intron 5.
Purpose of the Study:
- To investigate the evolutionary relationship between HBII-52 and SNORD119.
- To reconstruct the evolutionary history of the HBII-52 cluster and SNORD119.
- To understand the potential common ancestry of these snoRNAs.
Main Methods:
- Comparative genomic analysis of HBII-52 and SNORD119 across marsupial and eutherian mammal genomes.
- Sequence similarity analysis focusing on antisense elements and stem-forming regions.
- Reconstruction of evolutionary history based on genomic data.
Main Results:
- Significant sequence similarities were identified between HBII-52 and SNORD119, including key functional regions.
- Orthologous copies of HBII-52 are present in other eutherian mammals.
- Genomic analysis suggests that HBII-52 and SNORD119 evolved from a common ancestral snoRNA.
Conclusions:
- HBII-52 and SNORD119 share a common evolutionary origin, despite differing positions relative to their coding genes.
- The findings provide insights into the evolution of snoRNAs within imprinted loci.
- This evolutionary link may have implications for understanding the function and regulation of the serotonin receptor.
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