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Study IDs Variations in Black, White Genomes
Study IDs Variations in Not light, Pale GenomesTUESDAY, March 24 (HealthDay News) -- U.S. researchers possess identified 1,362 copy number variations (CNVs) in the human genome of blacks as well as 1,972 in whites. CNVs -- differences in gene copy numbers caused by deletions, duplications or rearrangements of genomic regions -- account for a large amount of human diversity as well as can as well as be associated with behavioral traits or increased susceptibility to a disease.
Across the genome, there was little difference in the frequency of CNVs between blacks as well as whites. But, there was a marked difference in the frequency of two duplications, one on chromosome 15 as well as another on chromosome 17, said Joseph P. McElroy as well as his colleagues in the neurology department at the University of California, San Francisco. A duplication in chromosome 17 (region 17q21) was found in 45% of the 435 whites in the study as well as in 8% of the 435 blacks. This region has been implicated in mental retardation caused by the deletion of two genes due to duplication. The two genes aren't located within the 17q21 region, but are very close to it, the researchers said. "It would be pleasant to know incase the CNV duplication of the region may possess an effect on the expression of these genes, which in turn could result in neurological disease. It is as well as interesting to find out whether the class of mental retardation associated with this locus is more ordinary in whites than in Africans or African-Americans. Incase this is real, then it may be one of the earliest reported diseases with differing ethnic frequencies due to CNVs," McElroy said in a news release. The study was published March 23 in the journal BMC Genetics. "To the best of our knowledge, this is the earliest detailed map of copy number variations in African-Americans. Understanding the distribution of CNVs in a population is a earliest step to addressing their role in disease," McElroy said. -- Robert Preidt SOURCE: BioMed Central, news release, March 23, 2009
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