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How can mutations in the excision repair process be produced from the xeroderma pigmentosum (XP) phenotype?...

How can mutations in the excision repair process be produced from the xeroderma pigmentosum (XP) phenotype? What is the "RNA World hypothesis"?

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How can mutations in the excision repair process be produced from the xeroderma pigmentosum (XP) phenotype?

Xerodrma pigmentosum is one of the autosomal recessive disorders where the ability of the DNA to repair the damage that has been caused by UV light is lost. In some of the extreme cases, complete sunlight exposure is forbidden. In normal cases, DNA damage would be occurring when there is UV light exposure. When there is high exposure to UV lights, this high energy light would be leading to pyrimidine dimers in the form cyclobutand pyrimidine dimers as well as pyrimidone photproducts. In the normal healthy being, this damage is excised with the help of endonucleases. The DNA pol would repair this by the use of ligase and would seal the transaction.

What is the "RNA World hypothesis"?

The RNA world hypothesis states that evolution happened in such a manner that due to the instability that RNA has, there was evolution of proteins as well as DNA since relatively RNA Was instable. Also, RNA had poorer catalytic properties and on a gradual form, there would be phasing out of the ribozymes. The RNA world hypothesis states that the ribosome is a one of the large complex molecule that would be assembling proteins . Though, the ribosome is composed of both protein component and the RNA component, it was found that the central mechanism of translation is catalysed only by RNA and is not catalysed by the proteins.


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