Elimination of two ribosome subunits activates cell cycle control

Alterations in the formation of ribosomes (the elements of the cell where proteins are made) cause the induction of p53 protein and cell cycle disruption. This process is crucial to understand fundamental biological processes and the emergence of various diseases. Now, scientists at the Bellvitge Biomedical Research Institute (IDIBELL) have found that this response is achieved independently, depending on which subunit of the ribosome (40S and 60S) is impaired, by the joint action of two proteins of the ribosome. The research results are published in the latest issue of the journal Genes and Development.

The , produced by the gene of the same name, is a in humans and other mammals. Half of human tumours have mutations in the and alterations of regulators of this gene are present in many other cancers. However, p53 is not only a tumour suppressor but is involved in other cellular processes such as longevity, mitochondrial oxidation and . Activation of p53 protein due to malfunctions in the formation of ribosomes is associated with several rare diseases that are linked with mutations in components of the cell nucleus.

The study by IDIBELL researchers shows that ribosomal proteins RPL11 and RPL5 cooperate to suppress Hdm2, another protein that regulates the degradation of p53. This causes increased levels of p53 and cell cycle arrest. These results are contrary to previous dogma, claiming that other ribosome proteins could elicit a similar response to RPL11 and RPL5.

The coordinator of the study, George Thomas, director of the research group of Metabolic Diseases and Cancer at IDIBELL explains that the knowledge of this mechanism "may have implications in understanding fundamental processes such as longevity, metabolic diseases or cancer and can provide a basis for developing new drugs."

add to favorites email to friend print save as pdf

Related Stories

Cancer is a p53 protein aggregation disease

Mar 29, 2011

Protein aggregation, generally associated with Alzheimer's and mad cow disease, turns out to play a significant role in cancer. In a paper published in Nature Chemical Biology, Frederic Rousseau and Joost Schymkowitz of VIB ...

Preventing cancer without killing cells

Mar 30, 2007

Inducing senescence in aged cells may be sufficient to guard against spontaneous cancer development, according to a paper published online this week in EMBO reports. It was previously unknown whether cellular senescence or ...

Recommended for you

Throwing a loop to silence gene expression

9 hours ago

All human cells contain essentially the same DNA sequence – their genetic information. How is it possible that shapes and functions of cells in the different parts of the body are so different? While every cell's DNA contains ...

A nucleotide change could initiate fragile X syndrome

Sep 01, 2014

Researchers reveal how the alteration of a single nucleotide—the basic building block of DNA—could initiate fragile X syndrome, the most common inherited form of intellectual disability. The study appears ...

Gene clues to glaucoma risk

Aug 31, 2014

Scientists on Sunday said they had identified six genetic variants linked to glaucoma, a discovery that should help earlier diagnosis and better treatment for this often-debilitating eye disease.

User comments