The protein that gives identical cells individuality

July 16, 2019

New insight into a protein's role in regulating tight DNA packing could have implications for combating tumor cell resistance to anti-cancer treatments.

Hokkaido University researchers have revealed how a protein maintains a delicate balance of tightly packing DNA inside yeast cells with the same genetic material, while also allowing for variation amongst them. The findings, published in the journal PLOS Genetics, could help researchers identify ways to suppress the formation of tumor cells that are resistant to anti-cancer drugs.

The incredibly long strands of DNA found in cells are packed into a structure called chromatin with the help of proteins called histones. Heterochromatin is where parts of chromatin are really tightly packed together. This makes certain genes difficult to access, effectively silencing them. Abnormal heterochromatin formation can inhibit genes that are essential for basic cell functions. But it can also play a role in cellular adaptation to changing circumstances by modifying gene accessibility. The mechanisms that regulate heterochromatin distribution are not yet fully understood.

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

When a fission yeast cell divides into two, each cell has identical genetic material. Murakami's team found that turning off Epe1 in yeast cells led to stochastic heterochromatin formation, altering the characteristics of some cells and leading to the production of a more diverse yeast population.

At the molecular level, Epe1 works against a molecular label on histone called H3K9me which recruits gene-silencing proteins for heterochromatin formation. The team found that Epe1 prevents H3K9me deposition at sites where abnormal "ectopic" heterochromatin has the potential to form. It also promotes the removal of H3K9me on already-formed ectopic heterochromatin, destabilizing the tight structure. "Interestingly, our study showed that the removal of ectopic heterochromatin by Epe1 is incomplete. Thus, it creates diversity in gene expression and cell characteristics in a population with the same genetic material," says Yota Murakami. "In other words, while Epe1 prevents the emergence of extreme diversity caused by accidental heterochromatin formation, it also allows individuality."

Cell diversity is thought to help adaptation to ever-changing environments, but, it is not always a good thing. Dividing tumor cells can also acquire diversity and develop resistance to anti-cancer treatments. "Since the chromatin regulatory mechanisms found in fission yeast cells are similar to those in humans and other mammals, this work could improve understandings of how cells in our body adapt to changing environments and develop resistance to anti-cancer treatments," explains Yota Murakami.

Hokkaido University

Related Tumor Cells Articles from Brightsurf:

Cancer researchers train white blood cells to attacks tumor cells
Scientists at the National Center for Tumor Diseases Dresden (NCT/UCC) and Dresden University Medicine, together with an international team of researchers, were able to demonstrate that certain white blood cells, so-called neutrophil granulocytes, can potentially - after completing a special training program -- be utilized for the treatment of tumors.

How to prevent the spread of tumor cells via the lymph vessels
Scientists from the German Cancer Research Center and the Mannheim Medical Faculty of the University of Heidelberg identified a new way to block the dangerous spread of tumor cells via lymphatic vessels.

The CNIO reprograms CRISPR system in mice to eliminate tumor cells without affecting healthy cells
CNIO researchers destroyed Ewing's sarcoma and chronic myeloid leukaemia tumor cells by using CRISPR to cut out the fusion genes that cause them.

Feeding off fusion or the immortalization of tumor cells
Despite all recent progress, cancer remains one of the deadliest human diseases.

How do tumor cells divide in the crowd?
Scientists led by Dr. Elisabeth Fischer-Friedrich, group leader at the Excellence Cluster Physics of Life (PoL) and the Biotechnology Center TU Dresden (BIOTEC) studied how cancer cells are able to divide in a crowded tumor tissue and connected it to the hallmark of cancer progression and metastasis, the epithelial-mesenchymal transition (EMT).

How tumor cells evade the immune defense
Scientists are increasingly trying to use the body's own immune system to fight cancer.

Engineered immune cells recognize, attack human and mouse solid-tumor cancer cells
CAR-T therapy has been used successfully in patients with blood cancers such as lymphoma and leukemia.

New pathway to attack tumor cells identified
A study led by the Institut de Neurociències (INc-UAB) describes a new strategy to tackle cancer, based on inducing a potent stress in tumor causing cell destruction by autophagy.

Nutrient deficiency in tumor cells attracts cells that suppress the immune system
A study led by IDIBELL researchers and published this week in the American journal PNAS shows that, by depriving tumor cells of glucose, they release a large number of signaling molecules.

Blocking sugar structures on viruses and tumor cells
During a viral infection, viruses enter the body and multiply in its cells.

Read More: Tumor Cells News and Tumor Cells Current Events is a participant in the Amazon Services LLC Associates Program, an affiliate advertising program designed to provide a means for sites to earn advertising fees by advertising and linking to