Posts about protein

The Amazing Reality of Genes and The History of Scientific Inquiry

cover of The Gene

The Gene by Siddhartha Mukherjee is a wonderful book. He does a great job of explaining the history of scientists learning about genes as well as providing understandable explanations for the current scientific understanding of genes and how they impact our lives.

As I have mentioned before, I find biology fascinating even though I found biology classes utterly boring and painful. I wish everyone could learn about biology with the insight people like Siddhartha Mukherjee provide. I realize not everyone is going to find the history and understanding of genes to be fascinating but for those who might this book is a great read. And don’t rule the idea out just because you found biology classes painful.

Life may be chemistry, but it’s a special circumstance of chemistry. Organisms exist not because of reactions that are possible, but because of reactions that are barely possible. Too much reactivity and we would spontaneously combust. Too little, and we would turn cold and die. Proteins enable these barely possible reactions, allowing us to live on the edges of chemical entropy – skating perilously, but never falling in.
– page 134

Whether it is the physics of our solar system or our biology there is a precarious band that allowed beings such as ourselves to evolve.

most genes, as Richard Dawkins describes them, are not “blueprints” but “recipes.” They do not specify parts, but processes; they are formulas, not forms. If you change a blueprint, the final product is change in a perfectly predictable manner: eliminate a widget specified in the plan, and you get a machine with a missing widget. But alteration of a recipe or formula doesn’t not change the product in a predictable manner: if you quadruple the amount of butter in a cake, the eventual effect is more complicated than just a quadruply buttered cake (try it; the whole thing collapses in an oily mess).
– page 454

The is a powerful idea. And when combined with turning genes on and off it is understandable how complex determining genetic impacts on biology and disease are. A few diseases or results (e.g. blue eyes) are nearly as simple as 1 or a few genes being altered in a specific way but most are not nearly so easy. And it isn’t like even that is so easy but with the amazing efforts scientists have made and the advanced tools those scientists created it can now seem simple to identify some such diseases.

The genetic code is universal. A gene from a blue whale can be inserted into a microscopic bacterium and it will be deciphered accurately and with near perfect fidelity. A corollary: there is nothing particularly special about human genes.
– page 480

This is something I have known and understood but it is still amazing. Genes and proteins and how they act to create the incredible diversity of life is something that is awe inspiring.

This book is a wonderful adventure for those interested in life and scientific inquiry.

Related: Epigenetics, Scientific Inquiry and UncertaintyHuman Gene Origins: 37% Bacterial, 35% Animal, 28% EukaryoticUnexpected Risks Found In Editing Genes To Prevent Inherited DisordersEpigenetic Effects on DNA from Living Conditions in Childhood Persist Well Into Middle AgeWhy Don’t All Ant Species Replace Queens in the Colony, Since Some Do

Defying Textbook Science, Study Finds Proteins Built Without DNA Instructions

Open any introductory biology textbook and one of the first things you’ll learn is that our DNA spells out the instructions for making proteins, tiny machines that do much of the work in our body’s cells. Results from a recent study show for the first time that the building blocks of a protein, called amino acids, can be assembled without blueprints – DNA and an intermediate template called messenger RNA (mRNA). A team of researchers has observed a case in which another protein specifies which amino acids are added.

“This surprising discovery reflects how incomplete our understanding of biology is,” says first author Peter Shen, Ph.D., a postdoctoral fellow in biochemistry at the University of Utah. “Nature is capable of more than we realize.”

To put the new finding into perspective, it might help to think of the cell as a well-run factory. Ribosomes are machines on a protein assembly line, linking together amino acids in an order specified by the genetic code. When something goes wrong, the ribosome can stall, and a quality control crew is summoned to the site. To clean up the mess, the ribosome is disassembled, the blueprint is discarded, and the partly made protein is recycled.

Yet this study reveals a surprising role for one member of the quality control team, a protein conserved from yeast to man named Rqc2. Before the incomplete protein is recycled, Rqc2 prompts the ribosomes to add just two amino acids (of a total of 20) – alanine and threonine – over and over, and in any order. Think of an auto assembly line that keeps going despite having lost its instructions. It picks up what it can and slaps it on.

“In this case, we have a protein playing a role similar to that filled by mRNA,” says Adam Frost, M.D., Ph.D., assistant professor at University of California, San Francisco (UCSF) and adjunct professor of biochemistry at the University of Utah. He shares senior authorship with Jonathan Weissman, Ph.D., a Howard Hughes Medical Institute investigator at UCSF, and Onn Brandman, Ph.D., at Stanford University. “I love this story because it blurs the lines of what we thought proteins could do.”

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Cancer Cells in Blind Mole Rats ‘commit suicide’

Cancer cells in blind mole rats ‘commit suicide’

Blind mole rats don’t get cancer, and geneticists have worked out why — their cells kill themselves with a poisonous protein when they multiply too much.

Blind mole rats, which live in underground burrows throughout Southern and Eastern Africa, and the Middle East, are fascinating creatures. The naked mole rat, in particular, is the only cold-blooded mammal known to man, doesn’t experience pain, and is also arguably the only mammal (along with the Damaraland mole rat) to demonstrate eusociality — that is, they live in large hierarchical communities with a queen and workers, like ants or bees.

They’re also cancer-proof, which was found in 2011 to be down to a gene that stops cancerous cells from forming. The same team thought that two other cancer-proof mole rat species might have similar genes, but instead it turns out that they do develop cancerous cells — it’s just that those cells are programmed to destroy themselves if they become dangerous.

Very interesting research. The results of evolution are amazing. And while turning the medical research discoveries into workable treatments for people is very difficult the continued increase in our knowledge helps us find treatments that work.

Related: Webcast of a T-cell Killing a Cancerous CellSynthetic Biologists Design a Gene that Forces Cancer Cells to Commit Suicide

Evolution Follows a Predictable Genetic Pattern

Far from random, evolution follows a predictable genetic pattern

The researchers carried out a survey of DNA sequences from 29 distantly related insect species, the largest sample of organisms yet examined for a single evolutionary trait. Fourteen of these species have evolved a nearly identical characteristic due to one external influence — they feed on plants that produce cardenolides, a class of steroid-like cardiotoxins that are a natural defense for plants such as milkweed and dogbane.

Though separated by 300 million years of evolution, these diverse insects — which include beetles, butterflies and aphids — experienced changes to a key protein called sodium-potassium adenosine triphosphatase, or the sodium-potassium pump, which regulates a cell’s crucial sodium-to-potassium ratio. The protein in these insects eventually evolved a resistance to cardenolides, which usually cripple the protein’s ability to “pump” potassium into cells and excess sodium out.

Andolfatto and his co-authors examined the sodium-potassium pump protein because of its well-known sensitivity to cardenolides. In order to function properly in a wide variety of physiological contexts, cells must be able to control levels of potassium and sodium. Situated on the cell membrane, the protein generates a desired potassium to sodium ratio by “pumping” three sodium atoms out of the cell for every two potassium atoms it brings in.

Cardenolides disrupt the exchange of potassium and sodium, essentially shutting down the protein, Andolfatto said. The human genome contains four copies of the pump protein, and it is a candidate gene for a number of human genetic disorders, including salt-sensitive hypertension and migraines. In addition, humans have long used low doses of cardenolides medicinally for purposes such as controlling heart arrhythmia and congestive heart failure.

Cool stuff. It makes sense to me which is nice (it is nice to get confirmation that I find what actually exists is sensible). When things that are true just seem crazy it is a bit disconcerting – like quantum mechanics. It is fun to read stuff that totally shakes up preconceived notions, but even then it is nice once I think understand it to find it sensible.

Related: All present-day Life on Earth Has A Single AncestorCambrian Explosion SongBacteriophages: The Most Common Life-Like Form on EarthMicrocosm by Carl Zimmer

2012 Nobel Prize in Chemistry to Robert Lefkowitz and Brian Kobilka

The Royal Swedish Academy of Sciences has decided to award the Nobel Prize in Chemistry for 2012 to

  • Robert J. Lefkowitz, Howard Hughes Medical Institute and Duke University Medical Center, Durham, NC, USA
  • and Brian K. Kobilka, Stanford University School of Medicine, Stanford, CA, USA

for studies of G-protein–coupled receptors.

Your body is a fine-tuned system of interactions between billions of cells. Each cell has tiny receptors that enable it to sense its environment, so it can adapt to new situtations. Robert Lefkowitz and Brian Kobilka are awarded the 2012 Nobel Prize in Chemistry for groundbreaking discoveries that reveal the inner workings of an important family of such receptors: G-protein–coupled receptors.

For a long time, it remained a mystery how cells could sense their environment. Scientists knew that hormones such as adrenalin had powerful effects: increasing blood pressure and making the heart beat faster. They suspected that cell surfaces contained some kind of recipient for hormones. But what these receptors actually consisted of and how they worked remained obscured for most of the 20th Century.

Lefkowitz started to use radioactivity in 1968 in order to trace cells’ receptors. He attached an iodine isotope to various hormones, and thanks to the radiation, he managed to unveil several receptors, among those a receptor for adrenalin: β-adrenergic receptor. His team of researchers extracted the receptor from its hiding place in the cell wall and gained an initial understanding of how it works.

The team achieved its next big step during the 1980s. The newly recruited Kobilka accepted the challenge to isolate the gene that codes for the β-adrenergic receptor from the gigantic human genome. His creative approach allowed him to attain his goal. When the researchers analyzed the gene, they discovered that the receptor was similar to one in the eye that captures light. They realized that there is a whole family of receptors that look alike and function in the same manner.

Today this family is referred to as G-protein–coupled receptors. About a thousand genes code for such receptors, for example, for light, flavour, odour, adrenalin, histamine, dopamine and serotonin. About half of all medications achieve their effect through G-protein–coupled receptors.

The studies by Lefkowitz and Kobilka are crucial for understanding how G-protein–coupled receptors function. Furthermore, in 2011, Kobilka achieved another break-through; he and his research team captured an image of the β-adrenergic receptor at the exact moment that it is activated by a hormone and sends a signal into the cell. This image is a molecular masterpiece – the result of decades of research.

Related: More details on the research2011 Nobel Prize in Chemistry2009 Nobel Prize in Chemistry: the Structure and Function of the RibosomeThe Nobel Prize in Chemistry 2008

Should Giant Viruses Be Included on the Tree of Life?

A new study of giant viruses supports the idea that viruses are ancient living organisms and not inanimate molecular remnants. The study may reshape the universal family tree, adding a fourth major branch to the three that most scientists agree represent the fundamental domains of life. But I am not sure that makes sense. The reason given for viruses not being “life” is that they cannot reproduce themselves – they hijack living cells to reproduce. The research in the past history of viruses as they evolved into current viruses is interesting but I don’t see the reason to classify current viruses as life.

The researchers used a relatively new method to peer into the distant past. Rather than comparing genetic sequences, which are unstable and change rapidly over time, they looked for evidence of past events in the three-dimensional, structural domains of proteins. These structural motifs, called folds, are relatively stable molecular fossils that – like the fossils of human or animal bones – offer clues to ancient evolutionary events, said University of Illinois crop sciences and Institute for Genomic Biology professor Gustavo Caetano-Anollés, who led the analysis.

“Just like paleontologists, we look at the parts of the system and how they change over time,” Caetano-Anollés said. Some protein folds appear only in one group or in a subset of organisms, he said, while others are common to all organisms studied so far.

“We make a very basic assumption that structures that appear more often and in more groups are the most ancient structures,” he said.

Most efforts to document the relatedness of all living things have left viruses out of the equation, Caetano-Anollés said.

“We’ve always been looking at the Last Universal Common Ancestor by comparing cells,” he said. “We never added viruses. So we put viruses in the mix to see where these viruses came from.”

The researchers conducted a census of all the protein folds occurring in more than 1,000 organisms representing bacteria, viruses, the microbes known as archaea, and all other living things. The researchers included giant viruses because these viruses are large and complex, with genomes that rival – and in some cases exceed – the genetic endowments of the simplest bacteria, Caetano-Anollés said.

Related: Plants, Unikonts, Excavates and SARsBacteriophages: The Most Common Life-Like Form on Earth8 Percent of the Human Genome is Old Virus GenesMicrobes Retroviruses

Open access paper: Giant Viruses Coexisted With the Cellular Ancestors and Represent a Distinct Supergroup Along With Superkingdoms Archaea, Bacteria and Eukarya

The discovery of giant viruses with genome and physical size comparable to cellular organisms, remnants of protein translation machinery and virus-specific parasites (virophages) have raised intriguing questions about their origin. Evidence advocates for their inclusion into global phylogenomic studies and their consideration as a distinct and ancient form of life.

Results call for a change in the way viruses are perceived. They likely represent a distinct form of life that either predated or coexisted with the last universal common ancestor (LUCA) and constitute a very crucial part of our planet’s biosphere.

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How do Plants Grow Into the Sunlight?

Plants are extremely competitive in gaining access to sunlight. A plant’s primary weapon in this fight is the ability to grow towards the light, getting just the amount it needs and shadowing its competition. Now, scientists have determined precisely how leaves tell stems to grow when a plant is caught in a shady place.

photo of a forest

Hole in the Wall trail, Olympic National Park, Washington, USA by John Hunter

The researchers discovered that a protein known as phytochrome interacting factor 7 (PIF7) serves as the key messenger between a plant’s cellular light sensors and the production of auxins, hormones that stimulate stem growth.

“We knew how leaves sensed light and that auxins drove growth, but we didn’t understand the pathway that connected these two fundamental systems,” says Joanne Chory, professor and director of the Salk’s Plant Biology Laboratory and a Howard Hughes Medical Institute investigator (HHMI provides huge amounts of funding for scientific research). “Now that we know PIF7 is the relay, we have a new tool to develop crops that optimize field space and thus produce more food or feedstock for biofuels and biorenewable chemicals.”

Plants gather intelligence about their light situation—including whether they are surrounded by other light-thieving plants—through photosensitive molecules in their leaves. These sensors determine whether a plant is in full sunlight or in the shade of other plants, based on the wavelength of red light striking the leaves. This is pretty cool; I love to learn about the brilliant strategies that have evolved.

If a sun-loving plant, such as thale cress (Arabidopsis thaliana), the species Chory studies, finds itself in a shady place, the sensors will tell cells in the stem to elongate, causing the plant to grow upwards towards sunlight.

When a plant remains in the shade for a prolonged period, however, it may flower early and produce fewer seeds in a last ditch effort to help its offspring spread to sunnier real estate. In agriculture, this response, known as shade avoidance syndrome, results in loss of crop yield due to closely planted rows of plants that block each other’s light.

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Exploring Eukaryotic Cells

This webcast is packed with information on the makeup and function of eukaryotic cells, which are the type of cells found in animals. It is part of a interesting series of science webcasts by Crash Course. The webcast style might be a bit too hyperactive and flippant for some but the content is quite interesting and the videos they are are of similar style and quality so if you like this one you can subscribe to their channel. They offer quite a few webcasts on science but they also offer webcasts on history.

Related: Plants, Unikonts, Excavates and SARsHow Cells AgeMidichloria mitochondrii

How Lysozyme Protein in Our Tear-Drops Kill Bacteria

A disease-fighting protein in our teardrops has been tethered to a tiny transistor, enabling UC Irvine scientists to discover exactly how it destroys dangerous bacteria. The research could prove critical to long-term work aimed at diagnosing cancers and other illnesses in their very early stages.

Ever since Nobel laureate Alexander Fleming found that human tears contain antiseptic proteins called lysozymes about a century ago, scientists have tried to solve the mystery of how they could relentlessly wipe out far larger bacteria. It turns out that lysozymes have jaws that latch on and chomp through rows of cell walls like someone hungrily devouring an ear of corn.

“Those jaws chew apart the walls of the bacteria that are trying to get into your eyes and infect them,” said molecular biologist and chemistry professor Gregory Weiss, who co-led the project with associate professor of physics & astronomy Philip Collins.

The researchers decoded the protein’s behavior by building one of the world’s smallest transistors – 25 times smaller than similar circuitry in laptop computers or smartphones. Individual lysozymes were glued to the live wire, and their eating activities were monitored.

“Our circuits are molecule-sized microphones,” Collins said. “It’s just like a stethoscope listening to your heart, except we’re listening to a single molecule of protein.”

It took years for the UCI scientists to assemble the transistor and attach single-molecule teardrop proteins. The scientists hope the same novel technology can be used to detect cancerous molecules. It could take a decade to figure out but would be well worth it, said Weiss, who lost his father to lung cancer.

“If we can detect single molecules associated with cancer, then that means we’d be able to detect it very, very early,” Weiss said. “That would be very exciting, because we know that if we treat cancer early, it will be much more successful, patients will be cured much faster, and costs will be much less.”

The project was sponsored by the National Cancer Institute and the National Science Foundation. Co-authors of the Science paper are Yongki Choi, Issa Moody, Patrick Sims, Steven Hunt, Brad Corso and Israel Perez.

Related: full press releaseWhy ‘Licking Your Wounds’ WorksHow Bleach Kills BacteriaAlgorithmic Self-Assembly

Healthy Diet, Healthy Living, Healthy Weight

Living and eating healthily is tricky but not entirely confusing. The whole area of eating healthy food and what is a healthy weight is one where the scientific inquiry process and the complexity of scientific research on what is healthy for us is clear. Scientists study various issues and learn things but creating simple rules has proven difficult. Different studies seem to show benefits of contradictory advice, advice once seen as wise is now seen as wrong…

This is an area I am far from knowledgable about. Still I try to pay some attention as I like being healthy. Being sick is the quickest way to appreciate how great it is to be healthy. From various things I have skimmed it seems there is more evidence from several studies about how difficult it is to lose weight. Our bodies seem to work against our efforts.

And this, it seems to me, makes the problem of increasing childhood and teen obesity even more important to deal with as soon as issues arise.

It seems to me the most important thing to take from this, is the importance of maintaining a healthy weight: since you can’t just easily make up for a bad year of weight gain. I am not sure why I haven’t seen this note in most of what I have read – I suspect it is our reluctance to make value judgements about what is healthy. The problem I see with that is, the best advice we have is confusing enough without people with more knowledge being reluctant to state their best advice given the current knowledge. That doesn’t mean the suggestions are right, but at least they are educated guesses.

I try to eat relatively healthily. Which for me means taking steps to increase the amount of vegetables I eat (especially greens and some fiber) and decrease the amount of sweets and heavily processed food I eat (I still eat way too much heavily processed food). And I try to exercise as it seems to have many benefits including helping make up for some weaknesses in your diet (like eating too many calories and too many “empty calories). In my opinion (which on this topic may well not be worth much) eating a bit more stuff that really isn’t so good for you and exercising more is an easier tradeoff than trying to eat perfectly and do the minimum amount of exercise needed to stay healthy.

I also eat yogurt – I like it and the beneficial benefits of some bacteria seems likely. I heard recently something that surprised me which is that the beneficial bacteria remain for close to 2 weeks. I figured they would be gone in a couple days. I only heard that from one source (I can’t remember now but some seemingly knowledgable source – scientist researching the area), so it might not be accurate but it was interesting.

Here is an example of one of these health studies. They find that a low protein diet resulted in a loss of “lean weight” (muscle…) and more fat than a comparable diet with more protein. The same weight with a higher percentage of fat is not a good thing for human health. Thus the message is that a lower protein diet has this risk that must be considered (and therefor higher protein diets may well be wise). Of course things get much more complicated than that when we actually try to live by a diet.

Effect of Dietary Protein Content on Weight Gain, Energy Expenditure, and Body Composition During Overeating

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Cancer Vaccines

A reader commented on a previous post (MIT Engineers Design New Type of Nanoparticle for Vacines) asking about how vaccines can fight cancer. Preventative vaccines can build up immune response to viruses which cause cancer. So the vaccine actually works against the virus which prevents the virus from causing cancer.

The U.S. Food and Drug Administration (FDA) has approved two vaccines, Gardasil® and Cervarix®, that protect against infection by the two types of human papillomavirus (HPV) – types 16 and 18 – that cause approximately 70% of all cases of cervical cancer worldwide. At least 17 other types of HPV are responsible for the remaining 30% of cervical cancer cases. HPV types 16 and/or 18 also cause some vaginal, vulvar, anal, penile, and oropharyngeal cancers.

Many scientists believe that microbes cause or contribute to between 15% and 25% of all cancers diagnosed worldwide each year, with the percentages being lower in developed than developing countries.

Vaccines can also help stimulate the immune system to fight cancers.

B cells make antibodies, which are large secreted proteins that bind to, inactivate, and help destroy foreign invaders or abnormal cells. Most preventive vaccines, including those aimed at hepatitis B virus (HBV) and human papillomavirus (HPV), stimulate the production of antibodies that bind to specific, targeted microbes and block their ability to cause infection. Cytotoxic T cells, which are also known as killer T cells, kill infected or abnormal cells by releasing toxic chemicals or by prompting the cells to self-destruct (a process known as apoptosis).

Other types of lymphocytes and leukocytes play supporting roles to ensure that B cells and killer T cells do their jobs effectively. These supporting cells include helper T cells and dendritic cells, which help activate killer T cells and enable them to recognize specific threats.

Cancer treatment vaccines are designed to work by activating B cells and killer T cells and directing them to recognize and act against specific types of cancer. They do this by introducing one or more molecules known as antigens into the body, usually by injection. An antigen is a substance that stimulates a specific immune response. An antigen can be a protein or another type of molecule found on the surface of or inside a cell.

Related: National Cancer Institute (USA)Nanoparticles With Scorpion Venom Slow Cancer SpreadUsing Bacteria to Carry Nanoparticles Into CellsGlobal Cancer Deaths to Double by 2030
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