Highly repetitive regions of junk DNA may be the key to a newly discovered mechanism for gene regulation.

The discovery during the Human Genome Project in the early 2000s that we humans have only about 20,000 protein-coding genes — about as many as the tiny soil-dwelling nematode worm, and less than half as many as the rice plant — came as a shock. That blow to our pride was softened, though, by the idea that the human genome is rich in regulatory connections. Our genes interact in a dense network, in which pieces of DNA and the molecules they encode (RNA and proteins) control the “expression” of other genes, influencing whether they make their respective RNA and proteins. To understand the human genome, we needed to understand this process of gene regulation.

That task, however, is proving to be much harder than decoding the sequence of the genome.

Initially, it was suspected that gene regulation was a simple matter of one gene product acting as an on/off switch for another gene, in digital fashion. In the 1960s, the French biologists François Jacob and Jacques Monod first elucidated a gene regulatory process in mechanistic detail: In Escherichia coli bacteria, when a repressor protein binds to a certain segment of DNA, it blocks the transcription and translation of an adjacent suite of genes that encode enzymes for digesting the sugar lactose. This regulatory circuit, which Monod and Jacob dubbed the lacoperon, has a neat, transparent logic.

A ‘lobby’ where a molecule mob tells genes what to do byPhilip Ball
Quanta 14 February 2024 – Read more