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Memory is Stored by Turning on Genes in Neurons (to Alter Connection Between Neurons)

Posted on December 28, 2011  Comments (0)

I find these kind of stories so interesting. I really have so little understanding of genes. I knew memory had something to do with altering connections between neurons. I had no idea that required turning on many genes in those neurons. Life really is amazing.

Neuroscientists identify a master controller of memory

When you experience a new event, your brain encodes a memory of it by altering the connections between neurons. This requires turning on many genes in those neurons.
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Lin and her colleagues found that Npas4 turns on a series of other genes that modify the brain’s internal wiring by adjusting the strength of synapses, or connections between neurons. “This is a gene that can connect from experience to the eventual changing of the circuit,” says [Yingxi] Lin

So far, the researchers have identified only a few of the genes regulated by Npas4, but they suspect there could be hundreds more. Npas4 is a transcription factor, meaning it controls the copying of other genes into messenger RNA — the genetic material that carries protein-building instructions from the nucleus to the rest of the cell. The MIT experiments showed that Npas4 binds to the activation sites of specific genes and directs an enzyme called RNA polymerase II to start copying them.

“Npas4 is providing this instructive signal,” Ramamoorthi says. “It’s telling the polymerase to land at certain genes, and without it, the polymerase doesn’t know where to go. It’s just floating around in the nucleus.”

When the researchers knocked out the gene for Npas4, they found that mice could not remember their fearful conditioning. They also found that this effect could be produced by knocking out the gene just in the CA3 region of the hippocampus. Knocking it out in other parts of the hippocampus, however, had no effect.

One of the things I aim to do in 2012 is read a few more books on biology and genes. I find it incredible what are genes actually are doing to allow us to live our lives. And I am also very ignorant on the whole area. So hopefully I can have some fun next year learning about it.

Related: Epigenetic Effects on DNA from Living Conditions in Childhood Persist Well Into Middle Age – Antigen Shift in Influenza Viruses – 8 Percent of the Human Genome is Old Virus Genes – Brain Reorganizes As It Learns Math

Epigenetic Effects on DNA from Living Conditions in Childhood Persist Well Into Middle Age

Posted on October 26, 2011  Comments (2)

Family living conditions in childhood are associated with significant effects in DNA that persist well into middle age, according to new research by Canadian and British scientists.

The team, based at McGill University in Montreal, University of British Columbia in Vancouver and the UCL Institute of Child Health in London looked for gene methylation associated with social and economic factors in early life. They found clear differences in gene methylation between those brought up in families with very high and very low standards of living. More than twice as many methylation differences were associated with the combined effect of the wealth, housing conditions and occupation of parents (that is, early upbringing) than were associated with the current socio-economic circumstances in adulthood. (1252 differences as opposed to 545).

I find Epigenetics to be a very interesting area. My basic understanding as I grew up was that you inherited your genes. But epigenetics explores how your genes change over time. This has been a very active area of research recently. Your DNA remains the same during your life. But the way those genes are expressed changes.

I don’t know of any research supporting the idea I mention in this example, but, to explain the concept in a simple way: you may carry genes in your DNA for processing food in different ways. If you have very limited diet the way your body reacts could be to express genes that specialize in maximizing the acquisition of nutrition from food. And it could be that your body sets these expressions based on your conditions when young; if later, your diet changes you may have set those genes to be expressed in a certain way. Again this is an example to try and explain the concept, not something where I know of research that supports evidence for this example.

The findings by these universities, were unfortunately published in a closed way. Universities should not support the closing of scientific knowledge. Several universities, that support open science, require open publication of scientific research. It is unfortunate some universities continue to support closed science.

The research could provide major evidence as to why the health disadvantages known to be associated with low socio-economic position can remain for life, despite later improvement in living conditions. The study set out to explore the way early life conditions might become ‘biologically-embedded’ and so continue to influence health, for better or worse, throughout life. The scientists decided to look at DNA methylation, a so-called epigenetic modification that is linked to enduring changes in gene activity and hence potential health risks. (Broadly, methylation of a gene at a significant point in the DNA reduces the activity of the gene.)

Related: DNA Passed to Descendants Changed by Your Life – Black Raspberries Alter Hundreds of Genes Slowing Cancer – Breastfeeding Linked to More Intelligent Kids

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Synthetic Biologists Design a Gene that Forces Cancer Cells to Commit Suicide

Posted on September 4, 2011  Comments (2)

Killing a cancer cell from the inside out

To create their tumor-killing program, the researchers designed a logic circuit — a system that makes a decision based on multiple inputs. In this case, the circuit is made of genes that detect molecules specific to a type of cervical cancer cell. If the right molecules are present, the genes initiate production of a protein that stimulates apoptosis, or programmed cell death. If not, nothing happens.

Because the genes used to create the circuits can be easily swapped in and out, this approach could also yield new treatments or diagnostics for many other diseases, according to Ron Weiss, an MIT associate professor of biological engineering and one of the leaders of the research team. “This is a general technology for disease-state detection,” he says.
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the researchers created a synthetic gene for a protein, called hBax, that promotes cell death. They designed the gene with two separate safeguards against the killing of healthy, non-HeLa cells: It can be turned off by high levels of microRNAs that are ordinarily low in HeLa, and can also be deactivated by low levels of microRNAs that are normally plentiful in HeLa. A single discrepancy from the target microRNA profile is enough to shut off production of the cell-death protein.

If all microRNA levels match up with the HeLa profile, the protein is produced and the cell dies. In any other cell, the protein never gets made, and the synthetic genes eventually break down.

More very cool research. It is exciting to see how much can be done when we invest in science and engineering research. Of course the path from initial research to implemented solutions is long and complex and often fails to deliver on the initial hopes. But some remarkable breakthroughs achieve spectacular results that we benefit from every day.

Related: Cancer Vaccines – Researchers Find Switch That Allows Cancer Cells to Spread – Global Cancer Deaths to Double by 2030 – Cloned Immune Cells Clear Patient’s Cancer

Most Genes? A crustacean the size of a grain of rice

Posted on February 8, 2011  Comments (4)

photo of Daphnia, a crustacean

“Daphnia are ubiquitous in freshwater ponds and lakes and are often used to assess the health of ponds. Since the creature is so well studied by ecologists, knowing its genetics should reveal a lot about how genes respond to different environments.

The first scientists to describe Daphnia thought they were a kind of flea because they assumed the red color came from sucking blood as fleas do. It turns out they’re not bloodsuckers – they’re blood makers. Daphnia have genes that make hemoglobin, so when the animal is stressed out, those genes switch on and the animal looks red.

In fact Daphnia have an astonishingly large number of genes. “We count more than 31,000 genes,” says [John] Colbourne. By comparison, the human genome has more like 23,000 genes. If Guinness tracks such things, Daphnia would hold the record for the most genes of any animal studied to date.

“Many of those genes – we estimate around 35 percent of them – are brand new to science,”

Daphnia can grow its own spear and helmet when threatened by an attacker

Related: Our Genome Changes as We Age – Amazing Designs of Life – One Species’ Genome Discovered Inside Another Species – Bdelloid Rotifers Abandoned Sex 100 Million Years Ago

All present-day Life on Earth Has A Single Ancestor

Posted on June 21, 2010  Comments (2)

All present-day life arose from a single ancestor

All life on Earth shares a single common ancestor, a new statistical analysis confirms.
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Because microorganisms of different species often swap genes, some scientists have proposed that multiple primordial life forms could have tossed their genetic material into life’s mix, creating a web, rather than a tree of life.
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A universal common ancestor is at least 102,860 times more probable than having multiple ancestors, Theobald calculates.
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For his analysis, Theobald selected 23 proteins that are found across the taxonomic spectrum but have structures that differ from one species to another. He looked at those proteins in 12 species – four each from the bacterial, archaeal and eukaryotic domains of life.

Then he performed computer simulations to evaluate how likely various evolutionary scenarios were to produce the observed array of proteins. Theobald found that scenarios featuring a universal common ancestor won hands down against even the best-performing multi-ancestor models.

Very interesting. Surprising too. As the article points out this doesn’t mean all life ever on Earth evolved from the single ancestor – life that has gone extinct could be from outside this single “tree.”

Related: Viruses and What is Life – Evolution is Fundamental to Science – Bacteria “Feed” on Earth’s Ocean-Bottom Crust

A Breakthrough Cure for Ebola

Posted on May 31, 2010  Comments (0)

A breakthrough cure for Ebola By Steven Salzberg

Last week, in what may be the biggest medical breakthrough of its kind in years, a group of scientists published results in The Lancet describing a completely new type of anti-viral treatment that appears to cure Ebola. They report a 100% success rate, although admittedly the test group was very small, just 4 rhesus monkeys.

This is a breakthrough not only because it may give us a cure for an uncurable, incredibly nasty virus, but also because the same method might work for other viruses, and because we have woefully few effective antiviral treatments. We can treat bacterial infections with antibiotics, but for most viruses, we have either a vaccine or nothing. And a vaccine, wonderful as it is, doesn’t help you after you’re already infected.

The scientists, led by Thomas Geisbert at Boston University, used a relatively new genomics technique called RNA interference to defeat the virus. Here’s how it works.
First, a little background: the Ebola virus is made of RNA, just like the influenza virus. And just like influenza, Ebola has very few genes – only 8. One of its genes, called L protein, is responsible for copying the virus itself. Two others, called VP24 and VP35, interfere with the human immune response, making it difficult for our immune system to defeat the virus.

Geisbert and his colleagues (including scientists from Tekmira Pharmaceuticals and USAMRIID) designed and synthesized RNA sequences that would stick to these 3 genes like glue. How did they do that? We know the Ebola genome’s sequence – it was sequenced way back in 1993. And we know that RNA sticks to itself using the same rules that DNA uses. This knowledge allowed Geisbert and colleagues to design a total of 10 pieces of RNA (called “small interfering RNA” or siRNA) that they knew would stick to the 3 Ebola genes. They also took care to make sure that their sticky RNA would not stick to any human genes, which might be harmful. They packaged these RNAs for delivery by inserting them into nanoparticles that were only 81-85 nanometers across.
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Related: Science Explained: RNA Interference – Amazing Science: Retroviruses – Ebola Outbreak in Uganda (Dec 2007)

Essentials of Genetics Website Reference

Posted on May 24, 2010  Comments (1)

Scitable is a science library and personal learning tool on genetics developed by Nature. I must admit I am against the closed science stance Nature normally supports. But this is a good effort on their part at actually talking advantage of the internet to openly promote science. I imagine Nature will eventually more and more move toward supporting open science.

The website has a library of over 200 faculty-written, peer-reviewed articles on core concepts in genetics, plus a video-based online primer called Essentials of Genetics, glossaries, spotlights on key issues, and lots more high quality faculty and student resources.

Scitable is a great place to research and learn more about genetics topics such as diseases, evolution, genetics and society.

Related: Gene Duplication and Evolution – DNA Passed to Descendants Changed by Your Life – Anger at Anti-Open Access Press Strategy

What Dogs Reveal About Evolution

Posted on January 17, 2010  Comments (0)

cover of the Greatest Show on Earth by Richard Dawkins

From, The Greatest Show on Earth: The Evidence for Evolution by Richard Dawkins

All breeds of dogs are domesticated wolves: not jackals, not coyotes and not foxes.
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Coppinger points out that when domestic animals break free and go feral for many generations, they usually revert to something close to their wild ancestor. We might expect feral dogs, therefore, to become rather wolf-like. But this doesn’t happen. Instead, dogs left to go feral seem to become the ubiquitous “village dogs” – “pye-dogs” – that hang around human settlements all over the Third World. This encourages Coppinger’s belief that the dogs on which human breeders finally went to work were wolves no longer. They had already changed themselves into dogs: village dogs, pye-dogs, perhaps dingos.

Real wolves are pack hunters. Village dogs are scavengers that frequent middens and rubbish dumps.
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Belyaev and his colleagues (and successors, for the experimental programme continued after his death) subjected fox cubs to standardised tests in which an experimenter would offer a cub food by hand, while trying to stroke or fondle it. The cubs were classified into three classes. Class III cubs were those that fled from or bit the person. Class II cubs would allow themselves to be handled, but showed no positive responsiveness to the experimenters. Class I cubs, the tamest of all, positively approached the handlers, wagging their tails and whining. When the cubs grew up, the experimenters systematically bred only from this tamest class.

After a mere six generations of this selective breeding for tameness, the foxes had changed so much that the experimenters felt obliged to name a new category, the “domesticated elite” class, which were “eager to establish human contact, whimpering to attract attention and sniffing and licking experimenters like dogs.” At the beginning of the experiment, none of the foxes were in the elite class. After ten generations of breeding for tameness, 18 per cent were “elite”; after 20 generations, 35 per cent; and after 30 to 35 generations, “domesticated elite” individuals constituted between 70 and 80 per cent of the experimental population.
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The tame foxes not only behaved like domestic dogs, they looked like them. They lost their foxy pelage and became piebald black and white, like Welsh collies. Their foxy prick ears were replaced by doggy floppy ears. Their tails turned up at the end like a dog’s, rather than down like a fox’s brush. The females came on heat every six months like a bitch, instead of every year like a vixen. According to Belyaev, they even sounded like dogs.

These dog-like features were side- effects. Belyaev and his team did not deliberately breed for them, only for tameness.

The famous domesticated silver fox experiment offers interesting insight into animal traits and evolution.

Related: The Selfish Gene by Richard Dawkins – The Evolution of House Cats – Darwin’s Beetles Still Producing Surprises – Backyard Wildlife: Fox

Microcosm by Carl Zimmer

Posted on December 26, 2009  Comments (0)

cover of Microcosm by Carl Zimmer

Microcosm: E. Coli and the New Science of Life by Carl Zimmer is an excellent book. It is full of fascinating information and as usual Carl Zimmer’s writing is engaging and makes complex topics clear.

E-coli keep the level of oxygen low in the gut making the resident microbes comfortable. At any time a person will have as many as 30 strains of E. coli in their gut and it is very rare for someone ever to be free of E. coli. [page 53]

In 1943, Luria and Delbruck published the results that won them the 1969 Nobel Prize in Physiology or Medicine in which they showed that bacteria and viruses pass down their traits using genes (though it took quite some time for the scientific community at large to accept this). [page 70]

during a crisis E coli’s mutation rates could soar a hundred – or even a thousandfold… Normally, natural selection favors low mutation rates, since most mutations are harmful. But in times of stress extra mutations may raise the odds that organisms will hit on a way out of their crisis… [alternatively, perhaps] In times of stress, E coli. may not be able to afford the luxury of accurate DNA repair. Instead, it turns to the cheaper lo-fi polymerases. While they may do a sloppier job, E coli. comes out ahead [page 106]
Hybridization is not the only way foreign DNA got into our cells. Some 3 billion years ago our single-celled ancestors engulfed oxygen-breathing bacteria, which became the mitochondria on which we depend. And, like E. coli, our genomes have taken in virus upon virus. Scientists have identified more than 98,000 viruses in the human genome, along with our mutant vestiges of 150,00 others… If we were to strip out all our transgenic DNA, we would become extinct.

I highly recommend Microcosm, just as I highly recommend Parasite Rex, by Carl Zimmer.

Related: Bacteriophages: The Most Common Life-Like Form on Earth – Foreign Cells Outnumber Human Cells in Our Bodies – Amazing Designs of Life – Amazing Science: Retroviruses – One Species’ Genome Discovered Inside Another’s

Science Explained: RNA Interference

Posted on November 13, 2009  Comments (1)

Explained: RNA interference

Every high school biology student learns the basics of how genes are expressed: DNA, the cell’s master information keeper, is copied into messenger RNA, which carries protein-building instructions to the ribosome, the part of the cell where proteins are assembled.

But it turns out the picture is far more complicated than that. In recent years, biologists have discovered a myriad of other molecules that fine-tune this process, including several types of RNA (ribonucleic acid). Through a naturally occurring phenomenon known as RNA interference, short strands of RNA can selectively intercept and destroy messenger RNA before it delivers its instructions.
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Double-stranded RNA molecules called siRNA (short interfering RNA) bind to complementary messenger RNA, then enlist the help of proteins, the RNA-induced silencing complex. Those proteins cleave the chemical bonds holding messenger RNA together and prevent it from delivering its protein-building instructions.

This article from MIT is one, of many, showing MIT’s commitment to science education of the public. Good job, MIT.

Related: Antigen Shift in Influenza Viruses – Posts explaining scientific principles and concepts – DNA Passed to Descendants Changed by Your Life – Why Does Hair Turn Grey as We Age? – Amazing Science: Retroviruses

The Only Known Cancerless Animal

Posted on October 28, 2009  Comments (6)

Unlike any other mammal, naked mole rate communities consist of queens and workers more reminiscent of bees than rodents. Naked mole rats can live up to 30 years, which is exceptionally long for a small rodent. Despite large numbers of naked mole-rats under observation, there has never been a single recorded case of a mole rat contracting cancer, says Gorbunova. Adding to their mystery is the fact that mole rats appear to age very little until the very end of their lives.

The mole rat’s cells express p16, a gene that makes the cells “claustrophobic,” stopping the cells’ proliferation when too many of them crowd together, cutting off runaway growth before it can start. The effect of p16 is so pronounced that when researchers mutated the cells to induce a tumor, the cells’ growth barely changed, whereas regular mouse cells became fully cancerous.

“It’s very early to speculate about the implications, but if the effect of p16 can be simulated in humans we might have a way to halt cancer before it starts.” says Vera Gorbunova, associate professor of biology at the University of Rochester and lead investigator on the discovery.

In 2006, Gorbunova discovered that telomerase—an enzyme that can lengthen the lives of cells, but can also increase the rate of cancer—is highly active in small rodents, but not in large ones.

Until Gorbunova and Seluanov’s research, the prevailing wisdom had assumed that an animal that lived as long as we humans do needed to suppress telomerase activity to guard against cancer. Telomerase helps cells reproduce, and cancer is essentially runaway cellular reproduction, so an animal living for 70 years has a lot of chances for its cells to mutate into cancer, says Gorbunova. A mouse’s life expectancy is shortened by other factors in nature, such as predation, so it was thought the mouse could afford the slim cancer risk to benefit from telomerase’s ability to speed healing.

While the findings were a surprise, they revealed another question: What about small animals like the common grey squirrel that live for 24 years or more? With telomerase fully active over such a long period, why isn’t cancer rampant in these creatures?

Related posts: Nanoparticles With Scorpion Venom Slow Cancer Spread – posts on university research – Gene Duplication and Evolution – Global Cancer Deaths to Double by 2030
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