ArticleNucleic acids research1994
A young Alu subfamily amplified independently in human and African great apes lineages.
Article in Nucleic acids research, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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15 citing papers in PubMed, 32 citations in OpenAlex.
- Structural divergence between the human and chimpanzee genomes.Human genetics · 2007Review
- Under the genomic radar: the stealth model of Alu amplification.Genome research · 2005Article
- Polymorphisms within a polymorphism: SNPs in and around a polymorphic Alu insertion in intron 44 of the human dystrophin gene.Journal of human genetics · 2004Article
- Comprehensive analysis of two Alu Yd subfamilies.Journal of molecular evolution · 2003Article
- Inactivation of CMP-N-acetylneuraminic acid hydroxylase occurred prior to brain expansion during human evolution.Proceedings of the National Academy of Sciences of the United States of America · 2002Article
- Molecular characterization of the pericentric inversion that causes differences between chimpanzee chromosome 19 and human chromosome 17.American journal of human genetics · 2002Article
- Phylogenetic and familial estimates of mitochondrial substitution rates: study of control region mutations in deep-rooting pedigrees.American journal of human genetics · 2001Article
- Alu-mediated inactivation of the human CMP- N-acetylneuraminic acid hydroxylase gene.Proceedings of the National Academy of Sciences of the United States of America · 2001Article
- Reading between the LINEs: human genomic variation induced by LINE-1 retrotransposition.Genome research · 2000Article
- Plasticity in the organization and sequences of human KIR/ILT gene families.Proceedings of the National Academy of Sciences of the United States of America · 2000Article
- Duplication of seven exons in the lysyl hydroxylase gene is associated with longer forms of a repetitive sequence within the gene and is a common cause for the type VI variant of Ehlers-Danlos syndrome.American journal of human genetics · 1997Article
- Characterization of species-specifically amplified SINEs in three salmonid species--chum salmon, pink salmon, and kokanee: the local environment of the genome may be important for the generation of a dominant source gene at a newly retroposed locus.Journal of molecular evolution · 1996Article
- Divergent intron arrangement in the MB1/LMP7 proteasome gene pair.Immunogenetics · 1996Article
- Standardized nomenclature for Alu repeats.Journal of molecular evolution · 1996Article
- Genetic variation of recent Alu insertions in human populations.Journal of molecular evolution · 1996Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A variety of Alu subfamilies amplified in primate genomes at different evolutionary time periods. Alu Sb2 belongs to a group of young subfamilies with a characteristic two-nucleotide deletion at positions 65/66. It consists of repeats having a 7-nucleotide duplication of a sequence segment involving positions 246 through 252. The presence of Sb2 inserts was examined in five genomic loci in 120 human DNA samples as well as in DNAs of higher primates. The lack of the insertional polymorphism seen at four human loci and the absence of orthologous inserts in apes indicated that the examined repeats retroposed early in the human lineage, but following the divergence of great apes. On the other hand, similar analysis of the fifth locus (butyrylcholinesterase gene) suggested contemporary retropositional activity of this subfamily. By a semi-quantitative PCR, using a primer pair specific for Sb2 repeats, we estimated their copy number at about 1500 per human haploid genome; the corresponding numbers in chimpanzee and gorilla were two orders of magnitude lower, while in orangutan and gibbon the presence of Sb2 Alu was hardly detectable. Sequence analysis of PCR-amplified Sb2 repeats from human and African great apes is consistent with the model in which the founding of Sb2 subfamily variants occurred independently in chimpanzee, gorilla and human lineages.
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