HOUSTON (June 21, 2009) Rearrangements of all sizes in genomes, genes and exons can result from a glitch in DNA copying that occurs when the process stalls at a critical point and then shifts to a different genetic template, duplicating and even triplicating genes or just shuffling or deleting part of the code within them, said researchers from Baylor College of Medicine in a recent report in the journal Nature Genetics. The report further elucidated the effect of the fork stalling and template switching mechanism involved in some forms of copy number variation.
"I think this is going to make people think very hard about copy number variation with respect to genome evolution, gene evolution and exon shuffling," said Dr. James R. Lupski (http://www.bcm.edu/genetics/facultyaz/lupski.html) , vice chair of molecular and human genetics at BCM and senior author of the report.
The mechanism not only represents a newly discovered method by which the genome generates copy number variation among genes, but it also demonstrates that copy number variation can occur at a different time in the life of a cell. DNA replication takes place as the cell is dividing and becoming two a process known as mitosis.
Copy number variation involves structural changes in the human genome that result in the deletion of genes or parts of them or extra copies of genes. Often, this process is associated with disease or with evolution of the genome itself.
DNA (deoxyribonucleic acid) exists as two complementary strands that remain together because of the attraction between nucleotides. A, or adenine, is always attracted to T, or thymine. C, or cytosine, is always attracted to G, or guanine.
When a cell divides, it must reproduce its DNA so that each cell that results from the division has the same genetic code. That means it must replicate its DNA. During this process, an enz
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Baylor College of Medicine