However, there are important points in an organism’s life when these marks benefit from being removed so that certain genes can be accessed and transcribed.

The methylation marks from the parent cells must be removed so that certain genes can be accessed and transcribed for the zygote to mature into a fully grown organism.

The TET3 protein works to demethylate the genome of the fertilized zygote to allow it to grow into a fully developed organism.

[7] While there is not much work regarding the role of Tet3 in humans, studies have been done on model organisms such as mice, frogs, and rats.

The study shows that TET3 as well as its product, 5-hydroxymethylcytosine (5hmC), are expressed more after focal ischemia in order to demethylate and turn on genes associated with DNA repair in neurons.

While the complete knockout of Tet3 appears to be fatal to the developing zygote, the mutation of one or more alleles of Tet3 can result in viable offspring.

[9] These mutations of Tet3 can greatly affect the TET3 protein and lead to a class of neurodevelopmental disorders in humans known as Beck–Fahrner syndrome.

[9] This article incorporates text from the United States National Library of Medicine, which is in the public domain.