Need help preparing for the Biology section of the MCAT? MedSchoolCoach expert, Ken Tao, will teach everything you need to know about Heterochromatin vs. Euchromatin, Telomeres and Centromeres of Eukaryotic Chromosome Organization. Watch this video to get all the MCAT study tips you need to do well on this section of the exam!

Recall that eukaryotic chromosomes are long strands of DNA molecules that contain the genetic information of an organism. They are located within the nucleus of the cell, and are composed of several structures. Once such structure is chromatin, which is a complex of DNA and protein packaged into a compact form that makes up the overall chromosome molecule. Remember that chromatin forms from DNA wrapped around histone proteins. There are two primary varieties of chromatin that are important to understand for the MCAT exam: Heterochromatin and euchromatin.

The main difference between the heterochromatin and euchromatin structures is how densely packed the chromatin fibers are. In euchromatin, the fibers are lightly packed. In this way, the DNA of euchromatin is accessible by RNA polymerase, and it can be actively transcribed. Heterochromatin, on the other hand, has densely packed chromatin. Unlike euchromatin, RNA polymerase cannot access the DNA in heterochromatin, and it cannot be transcribed.

Heterochromatin

Heterochromatin exists in two distinct forms. One is called constitutive heterochromatin, which is always in a heterochromatin state. In this way, constitutive heterochromatin is never transcribed and generally consists of repetitive DNA sequences with structural roles. Some examples of constituent heterochromatin include centromeres, as well as telomeres.

The other form of heterochromatin is called facultative heterochromatin. Facultative heterochromatin can switch between a heterochromatin and euchromatin state, depending on the conditions. This type of heterochromatin may include coding regions in which the gene expression has been turned off. However, there are several ways facultative heterochromatin can switch between the inactive and active forms.

One method for how facultative heterochromatin can become euchromatin is through histone acetylation and deacetylation. Recall, DNA has a negative charge, and it is attracted to the positive charge of histone proteins. Histone acetylation will add an acetyl group to the side chains of the positively charged basic amino acids. This action removes the positive charge, weakening the attractive electrostatic interaction between DNA and histone proteins. This process makes the chromatin less densely packed and converts the heterochromatin into euchromatin, and the gene can now be expressed.

Similarly, the opposite process of histone acetylation or histone deacetylation can occur. Instead of adding acetyl groups, histone deacetylation will remove acetyl groups. This process will reintroduce the positive charge onto the histone protein and turn euchromatin into facultative heterochromatin.

In terms of altering gene expression, aside from acetylation, another way this is done is through DNA methylation. Generally, DNA methylation, or the addition of methyl groups on DNA molecules, results in silencing gene expression. An important example of DNA methylation is the inactivation of one of the two X chromosomes in female egg cells.

Telomeres & Centromeres

Recall that telomeres are repetitive sequences at the ends of chromosomes. Telomeres are a form of constitutive heterochromatin, and they have a structural role. They protect the ends of DNA from degradation, and they also prevent DNA from shortening during DNA replication. Remember that during DNA replication, there is an end replication problem in which the ends of the DNA cannot be fully replicated in the lagging strand. Usually, two telomeres will also shorten in sequence, but this is prevented by the telomerase enzyme that will extend the telomere sequence. As an aside, studies have shown that cellular aging and tumor formation may be related to telomere shortening. However, researchers are still unsure if telomere shortening is causing aging and disease, or is a result of these things.

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