[Press release] Jumping genes have essential biological functions

From the 19 February 2015 EurekAlert!

“Alu” sequences are small repetitive elements representing about 10% of our genome. Because of their ability to move around the genome, these “jumping genes” are considered as real motors of evolution. However, they were considered for a long time as “junk” DNA, because, although they are transcribed into RNA, they encode no proteins and do not seem to participate actively in the cell’s functions. Now, the group of Katharina Strub, professor at the Faculty of Science of the University of Geneva (UNIGE), Switzerland, has uncovered two key functions of Alu RNAs in human cells, which are the subject of two different articles published in Nucleic Acids Research. Alu RNA can bind to specific proteins forming a complex called Alu RNP. On the one hand, this complex allows the cells to adapt to stress caused for example by chemical poisoning or viral infection. On the other hand, the same complex plays a role in protein synthesis by regulating the number of active ribosomes, suggesting that it could be part of the innate system of cellular defense against certain viruses.

 

[Press release] Connection between childhood adversity and psychiatric disorders seen at cellular level | EurekAlert! Science News

Connection between childhood adversity and psychiatric disorders seen at cellular level | EurekAlert! Science News.

Logo for mitochondrial DNA (Photo credit: Wikipedia)

From the 20 January 2015 press release

PROVIDENCE, R.I. – In a new study published online in Biological Psychiatry on January 16, 2015, researchers from Butler Hospital identify an association between biological changes on the cellular level and both childhood adversity and psychiatric disorders. These changes in the form of telomere shortening and alterations of mitochondrial DNA (mtDNA), are important in the aging process, and this new research provides evidence that psychosocial factors–specifically childhood adversity and psychiatric disorders– may also influence these cellular changes and could lead to accelerated aging.

Mitochondria convert molecules from food into energy that can be used by cells and also play a key role in cellular growth, signaling, and death. Telomere shortening is also a measure of advanced cellular aging. Recent studies have examined the possible connection between mitochondria and psychiatric disorders, but the research is very limited, and no prior work has examined the relationship of mitochondrial DNA to psychosocial stress. “We are interested in these relationships because there is now clear evidence that stress exposure and psychiatric conditions are associated with inflammation and health conditions like diabetes and heart disease. Identifying the changes that occur at a cellular level due to these psychosocial factors allows us to understand the causes of these poor health conditions and possibly the overall aging process.” said Audrey Tyrka, MD, PhD, Director of the Laboratory for Clinical and Translational Neuroscience at Butler Hospital and Associate Professor of Psychiatry and Human Behavior at Brown University.

Related articles

• Childhood adversity, psychiatric disorders show advanced cellular ageing
• Link between Childhood Adversity, Psychiatric Disorders
• A Rough Childhood Can Literally Age You Says a New Study
• Development of psychosis: Gray matter loss and the inflamed brain
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[Press release] Why Scientists Are Blaming Cilia for Human Disease – Scientific American

Why Scientists Are Blaming Cilia for Human Disease – Scientific American.

Hairlike structures on cells may play a role in a host of genetic disorders, including kidney degeneration, vision impairment and even some cancers

December 10, 2014 |By Joshua A. Krisch

Hairlike cilia may be at the roots of of several genetic disorders.
Image Courtesy of StudyBlue.com

Scientists now believe that a number of genetic disorders, from polycystic kidney disease to some forms of retinal degeneration, can ultimately be traced back to cilia—bristly, hairlike structures that dot cell surfaces.

In a review article published in the December 1 BioScience, George B. Witman, a cellular biologist at the University of Massachusetts Medical School, highlighted the growing body of evidence that abnormal or absent cilia can cause a wide range of human disorders, dubbed “ciliopathies.”

“Kidney disease and blindness, multiple digits, shortened bones or extremities, obesity—all of these things, it turns out, are due to defects in cilia,” he says. Experts add that the discovery of a common thread between these disparate disorders may eventually help researchers develop gene-based therapies to combat those conditions.

At first blush, cilia seem relatively innocuous. As they beat back and forth outside the cell, coordinated brushes of so-called motile cilia regulate fluid flow nearby. But almost all human cells also have one primary, or nonmotile, cilium that functions more like a molecular antenna. The primary cilium is an internally dynamic structure, packed with proteins that detect and convey important messages to its cell about the local environment. “The signaling machinery is concentrated in the cilia,” Witman says. “All in this very tightly controlled, constrained space.”

…

Related articles

• Ciliopathies lie behind many human diseases

[News article] Ciliopathies lie behind many human diseases — ScienceDaily

Ciliopathies lie behind many human diseases — ScienceDaily.

Excerpt

Date:December 1, 2014

Source: American Institute of Biological Sciences

Summary: Growing interest in cilia, which are finger-like organelles that extend from the bodies of individual cells, has revealed their role in a number of human ailments. As a result of cilia’s presence in a wide variety of cells, defects in them cause diverse human diseases that warrant further study.

…

Cilia perform a broad range of functions, including a starring role in cell signalling. Motile ones wiggle and so move fluids within the body, including cerebrospinal fluid in the brain. In humans, cilia are found on almost every cell in the body. Because of this, ciliopathies often make themselves known as syndromes with widely varying effects on a number of tissue types. For instance, the ciliopathy Jeune asphyxiating thoracic dystrophy involves the development of abnormally short ribs, accompanied by short limbs and, occasionally, the development of extra digits.

In primary ciliary dyskinesia, motile cilia are dysfunctional and fail to beat. This can lead to bronchitis resulting from the failure to clear mucus from the sufferer’s airways. Male patients with primary ciliary dyskinesia are infertile because of impaired motility of the sperm’s flagellum (flagella and cilia are structurally similar).

The article’s authors point to a number of other human diseases in which cilia may play a role; for example, some cancers and neurological diseases may be related to ciliopathies. Because of the limitations placed on research involving humans, the authors propose the use of model species ranging from the green alga Chlamydomonas to the house mouse to further study the role of cilia. They write, “We can anticipate that new and improved techniques will open new avenues for gaining further insight into these immensely important and ever more fascinating cell organelles.”

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[Press release] Obesity: Not just what you eat

Obesity: Not just what you eat.

Tel Aviv University research shows fat mass in cells expands with disuse

Over 35 percent of American adults and 17 percent of American children are considered obese, according to the latest survey conducted by the Centers for Disease Control and Prevention. Associated with diabetes, heart disease, stroke, and even certain types of cancer, obesity places a major burden on the health care system and economy. It’s usually treated through a combination of diet, nutrition, exercise, and other techniques.

To understand how obesity develops, Prof. Amit Gefen, Dr. Natan Shaked and Ms. Naama Shoham of Tel Aviv University’s Department of Biomedical Engineering, together with Prof. Dafna Benayahu of TAU’s Department of Cell and Developmental Biology, used state-of-the-art technology to analyze the accumulation of fat in the body at the cellular level. According to their findings, nutrition is not the only factor driving obesity. The mechanics of “cellular expansion” plays a primary role in fat production, they discovered.

By exposing the mechanics of fat production at a cellular level, the researchers offer insight into the development of obesity. And with a better understanding of the process, the team is now creating a platform to develop new therapies and technologies to prevent or even reverse fat gain. The research was published this week in the Biophysical Journal.

Getting to the bottom of obesity

“Two years ago, Dafna and I were awarded a grant from the Israel Science Foundation to investigate how mechanical forces increase the fat content within fat cells. We wanted to find out why a sedentary lifestyle results in obesity, other than making time to eat more hamburgers,” said Prof. Gefen. “We found that fat cells exposed to sustained, chronic pressure — such as what happens to the buttocks when you’re sitting down — experienced accelerated growth of lipid droplets, which are molecules that carry fats.

“Contrary to muscle and bone tissue, which get mechanically weaker with disuse, fat depots in fat cells expanded when they experienced sustained loading by as much as 50%. This was a substantial discovery.”

The researchers discovered that, once it accumulated lipid droplets, the structure of a cell and its mechanics changed dramatically. Using a cutting-edge atomic force microscope and other microscopy technologies, they were able to observe the material composition of the transforming fat cell, which became stiffer as it expanded. This stiffness alters the environment of surrounding cells by physically deforming them, pushing them to change their own shape and composition.

“When they gain mass and change their composition, expanding cells deform neighboring cells, forcing them to differentiate and expand,” said Prof. Gefen. “This proves that you’re not just what you eat. You’re also what you feel — and what you’re feeling is the pressure of increased weight and the sustained loading in the tissues of the buttocks of the couch potato.”

The more you know …

“If we understand the etiology of getting fatter, of how cells in fat tissues synthesize nutritional components under a given mechanical loading environment, then we can think about different practical solutions to obesity,” Prof. Gefen says. “If you can learn to control the mechanical environment of cells, you can then determine how to modulate the fat cells to produce less fat.”

The team hopes that its observations can serve as a point of departure for further research into the changing cellular environment and different stimulations that lead to increased fat production.

Protecting the body in good times and bad

From the 15 July 2013 article at EurekAlert

Brandeis scientists bring us a step closer to understanding how to control cancer cells without harming healthy ones

The nasty side effects of radiation and chemotherapy are well known: fatigue, hair loss and nausea, to name a few. Cancer treatment can seem as harsh as the disease because it can’t differentiate healthy cells from cancerous cells, killing both.

But what if there were a way to control or stop the growth of cancer cells without harming other cells?

Brandeis biologist Michael T. Marr is one step closer to understanding how cells promote and inhibit protein synthesis — an essential part of cellular reproduction — during times of stress. His new paper, co-authored by graduate students Calla Olson, Marissa Donovan and Michael Spellberg, is published in eLife, an open access digital publication for life science and biomedicine research.

Marr and his team discovered a mechanism, like an emergency backup system, that allows cells to synthesize certain proteins while shutting down the production of others. Building proteins requires a chain reaction with a dozen moving parts, each triggering the next step. These chain reactions are called signaling pathways.

The pathway that interests Marr and his team is called the insulin and insulin-like receptor (IIS) pathway. It is part of the body’s emergency response system. When organisms are healthy and safe, the IIS pathway increases the activity of a protein complex called eIF4A, which helps in the synthesis of proteins.

But let’s say you’re not safe. You’re starving. Your body is being deprived of nutrients, forcing you to conserve energy and resources. The IIS pathway, sensitive to this stress, realizes something isn’t right, and sends a signal to stop eIF4A.

Protein synthesis screeches to a halt — for the most part.

Marr and his team discovered that the messages that build insulin receptor proteins have internal mechanisms allowing them to synthesize protein without the eIF4A kick-start. When the rest of the production line slows down, production of insulin receptors in the IIS ramps up. Why?

The hope is you’re about to find food. The insulin receptors help the IIS pathway recognize when it’s out of danger. The more receptors, the faster the IIS pathway can start ramping up protein production again. The same principle applies on the cellular level when cancerous cells overwhelm healthy cells, starving them of oxygen and nutrients — the healthy cells continue to produce insulin receptors.

“Even during times of stress, cells are stockpiling for good times,” says Marr.

The mechanism that allows synthesis of insulin receptors during stress is the same from flies to mammals, pointing to a response conserved in evolution, Marr says.

Though this research is still early, the more deeply scientists understand mechanisms involved in growth and inhibition, the better they can decipher diseases that rely on uncontrolled cell growth, like cancer.

Related articles

• Is There a Way to Control or Stop the Growth of Cancer Cells Without Harming Other Cells? (medindia.net)
• One Step Closer To Understanding How To Control Cancer Cells Without Harming Healthy Ones (medicalnewstoday.com)
• New Method of ‘Starving’ Cancer Cells Developed (medindia.net)
• Cancer cure just got closer: scientists harness our natural-born killers – the T cells – to target malign tumours (belfasttelegraph.co.uk)
• Treatment Offer New Hope in Quest for Non-Toxic Cancer Treatment (crystalcleandrinkingwaterblog.wordpress.com)
• Cancer’s Natural Enemy, Actually Starves It to Death (foodconsumer.org)

 

New Genetics Education Resource

Genetics, Education, Discovery

From a recent email (National Library of Medicine)

The National Library of Medicine (NLM)  is pleased to announce the release of a new educational resource, GeneEd.

..a useful resource for students and teachers in grades 9 – 12 to learn genetics.

GeneEd allows students and teachers to explore topics such as Cell Biology, DNA, Genes, Chromosomes, Heredity/Inheritance Patterns, Epigenetics/Inheritance and the Environment, Genetic Conditions, Evolution, Biostatistics, Biotechnology, DNA Forensics, and Top Issues in Genetics.

Teachers can use the site to introduce topics, supplement existing materials, and provide as a reliable source to students conducting research.

 

The site links to categories such as research articles, animation, games, videos, interactive tutorials, and labs and experiments. 3D images, illustrations and text from NHRGI help to enrich the user experience by providing vivid imagery to reinforce genetic concepts.

Text varies from easy-to-read to advanced reading levels, which makes this a versatile tool both in and out of the classroom.
Specialty pages including Teacher Resources and Labs and Experiments highlight those tools that teachers may find particularly helpful.

Other specialty pages such as Careers in Genetics and Highlights allow students to see what is new and noteworthy in the field of Genetics along with links to different careers related to the science of Genetics.

Related articles

• GeneEd (New Genetics Education Resource from the National Library of Medicine) (bluesyemre.com)
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• How much modern genetics should be learnt in school? (wellcometrust.wordpress.com)
• Personal genomics: where science fiction meets reality (csironewsblog.com)

Are Cancers Newly Evolved Species?

Staining chromosomes with different dyes highlights the orderly nature of the normal human karyotype (left), that is, humans have precisely two copies of each chromosome with no leftovers. A bladder cancer cell (right) has extra copies of some chromosomes, a few missing normal chromsomes, and a lot of hybrid or marker chromosomes, which characterize cancer cells. (Credit: Image courtesy of University of California – Berkeley)

From the 26 July 2011 Science Daily article

Cancer patients may view their tumors as parasites taking over their bodies, but this is more than a metaphor for Peter Duesberg, a molecular and cell biology professor at the University of California, Berkeley.

Cancerous tumors are parasitic organisms, he said. Each one is a new species that, like most parasites, depends on its host for food, but otherwise operates independently and often to the detriment of its host.

In a paper published in the July 1 issue of the journal Cell Cycle, Duesberg and UC Berkeley colleagues describe their theory that carcinogenesis — the generation of cancer — is just another form of speciation, the evolution of new species.

A molecular biologists has long believed that cancer results from chromosome disruption rather than a handful of gene mutations, which is the dominant theory today. That idea has led him to propose that cancers have actually evolved new chromosomal karyotypes that qualify them as autonomous species, akin to parasites and much different from their human hosts.

“Cancer is comparable to a bacterial level of complexity, but still autonomous, that is, it doesn’t depend on other cells for survival; it doesn’t follow orders like other cells in the body, and it can grow where, when and how it likes,” said Duesberg. “That’s what species are all about.”

This novel view of cancer could yield new insights into the growth and metastasis of cancer, Duesberg said, and perhaps new approaches to therapy or new drug targets. In addition, because the disrupted chromosomes of newly evolved cancers are visible in a microscope, it may be possible to detect cancers earlier, much as today’s Pap smear relies on changes in the shapes of cervical cells as an indication of chromosomal problems that could lead to cervical cancer.

Read the article