The protein that confers identical identities to cells – ScienceDaily

Researchers at Hokkaido University have revealed how a protein maintains a delicate balance of packing the DNA tightly in yeast cells with the same genetic material, while allowing variations between them. The results, published in the journal PLOS Genetics, could help researchers identify ways to suppress the formation of tumor cells resistant to anticancer drugs.

The very long DNA strands found in the cells are packaged in a structure called chromatin with the help of proteins called histones. The heterochromatin is the place where some parts of the chromatin are very closely related. This makes it difficult to access certain genes and silences them. Abnormal formation of heterochromatin may inhibit genes essential to basic cellular functions. But it can also play a role in adapting to changing circumstances by changing the accessibility of genes. The mechanisms that regulate the distribution of heterochromatin are not yet well understood.

A protein, called Epe1, is known for its suppressor role in the formation of heterochromatin. Yota Murakami, a biological chemist from Hokkaido University, led a team of scientists in Japan to find out what was going on at the molecular level.

When a yeast cell fission splits into two, each cell has identical genetic material. The Murakami team discovered that disabling Epe1 in yeast cells led to the stochastic formation of heterochromatin, altering the characteristics of certain cells and leading to the production of a larger yeast population. diversified.

At the molecular level, Epe1 acts against a molecular marker on the histone called H3K9me, which recruits genes inhibiting genes for the formation of heterochromatin. The team discovered that Epe1 prevents the deposition of H3K9me on sites where ectopic "abnormal heterochromatin" is likely to form. It also promotes the elimination of H3K9me on already formed ectopic heterochromatin, destabilizing the narrow structure. "It is interesting to note that our study showed that the extraction of ectopic heterochromatin by Epe1 is incomplete, so it creates a diversity in the expression of genes and cell characteristics in a population with the same genetic material, "says Yota Murakami. "In other words, although Epe1 prevents the emergence of extreme diversity caused by the accidental formation of heterochromatin, it also allows individuality."

Cell diversity is thought to facilitate adaptation to ever-changing environments, but this is not always a good thing. The division of tumor cells can also acquire diversity and develop resistance to cancer treatments. "Since the regulatory mechanisms of chromatin in fission yeast cells are similar to those in humans and other mammals, these works could shed some light on how our body's cells function." Adapt to changing environments and develop resistance to cancer treatments, "Yota Murakami explains.

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