Linkage Disequilibrium: A Case Study

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For a while, FTO has been known to associate with the gene for obesity in humans, however studies are explaining that this is not the case. The misunderstanding is coming from the LD block to FTO, LD is also known as linkage disequilibrium. Linkage disequilibrium is defined as “a state involving two loci in which the probability of a joint gamete is not equal to the product of the probabilities of the constituent genes. The difference between these quantities is the increase of the disequilibrium; there are many causes of the disequilibrium.” (Farlex Partner Medical Dictionary) The guess is that they are labeling SNPs for the reason, which has taken a turn toward inaccurate facts for the cis regulatory inputs. Thorough calculations…show more content…
The results lead that they were the cause of the manifestation of the traits of IRX3. “While Irx3 expression was detected in the actuate nucleus of the hypothalamus, three enhancer sequences isolated from the LD block drove expression in lung and several brain regions, but not in hypothalamus” (Rinkwitz 2015) The question that is lurking in the researchers mind were, does FTO intro 1 have any connection to the growth of the IRX3 gene regulatory? Therefore they introduced BAC, there after was transgenesis in Zebrafish. One of their concerns was the single nucleotide polymorphisms rs9939609; it is on the list of one of the main effects for excess over weight in human’s complete set of DNA. Which is also known as genome, “Genome contains all of the information needed to build and maintain that organism. In humans, a copy of the entire genome—more than 3 billion DNA base pairs—is contained in all cells that have a nucleus.” (Genetics Home Reference) SNP rs9939609 has been known to cause an increase in 3 kilograms weight gain on average in homozygous carriers. SNP rs9939609 is enclosed in the center of the LD block and it is 84 KB below the FTO promoter facing the rear of the 105 KB intron 1. “A BAC encompassing 183 kb of human genomic sequence including FTO upstream sequence and intron 1 in its entirety was modified by galK mediated homologous
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