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The human genome takes shape and shifts over time | Science News


If you could unravel all the DNA in a single human cell and stretch it out, you’d have a molecular ribbon about 2 meters long and 2 nanometers across. Now imagine packing it all back into the cell’s nucleus, a container only 5 to 10 micrometers wide. That would be like taking a telephone cord that runs from Manhattan to San Francisco and cramming it into a two-story suburban house.

Source: The human genome takes shape and shifts over time | Science News

The bare-naked ribbon of DNA is only the beginning of DNA organization, as elucidated in 1954, by Watson, Crick, their unsung assistant/collaborator Rosalind Franklin (an X-ray crystallographer whose pictures showed the helical structure of the basic base-paired ribbon but who died in 1957 at 37 of ovarian cancer), and Maurice Wilkins (who shared the Nobel prize with Watson and Crick.)

DNA is supported by proteins such as histones as well as many others; these proteins are used to wind the DNA (histones) and are attached at critical points to fold the DNA into structures that appose related genes that are turned on and off together.  This article in Science News describes the 3D structure of DNA as far as is known today, and more importantly, what is known today of how the structure changes over time and in different tissues (known as the 4D structure.)

This structure is important to individual cells, making it possible for the cell to organize the changes in DNA expression over time with altered circumstances.  A technique known as “Hi-C” allows scientists to discern which segments of DNA are close together at a particular moment in the life of the cell.  For example, proteins important to the circadian rhythm of the cell are produced in sequence depending on the time of day, and their DNA’s location in the nucleus also changes at the same time, moving closer together and farther apart as the day passes.  Most of these interactions are controlled by proteins called CTCF and cohesins.

Abnormalities in the shape of the nucleus are seen in normal aging, progeria, and in cancer, to give just a few examples.  It seems that progeria is related to abnormal folding of DNA; in one type, there is a mutation in lamin A, a set of proteins that support the normal structure of the membrane surrounding the nucleus, and in another type, a mutation expressed in WRN protein has a similar effect.  In “normal” aging, there is a similar problem with lamin A in a subpopulation of cells, while in this type of progeria the same problem with lamin A appears in every cell.

Discoveries that explain the effects of “normal aging” on the brain may be helpful to those with “normal aging” in a surprising way.

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