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The Amazing Reality of Genes and The History of Scientific Inquiry

Posted on March 4, 2017  Comments (4)

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 Uncertainty – Human Gene Origins: 37% Bacterial, 35% Animal, 28% Eukaryotic – Unexpected Risks Found In Editing Genes To Prevent Inherited Disorders – Epigenetic Effects on DNA from Living Conditions in Childhood Persist Well Into Middle Age – Why Don’t All Ant Species Replace Queens in the Colony, Since Some Do

An Eukaryote that Completely Lacks Mitochondria

Posted on June 11, 2016  Comments (0)

If you don’t have any idea what the title means that is ok. I probably wouldn’t have until the last 15 years when I found how interesting biology is thanks to the internet and wonderful resources online making biology interesting. I hope you find learning about biology as interesting as I do.

Look, Ma! No Mitochondria

Mitochondria have their own DNA, and scientists believe they were once free-living bacteria that got engulfed by primitive, ancient cells that were evolving to become the complex life forms we know and love today.
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What they learned is that instead of relying on mitochondria to assemble iron-sulfur clusters, these cells use a different kind of machinery. And it looks like they acquired it from bacteria.

The researchers say this is the first example of any eukaryote that completely lacks mitochondria.
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However, the results do not negate the idea that the acquisition of a mitochondrion was an important and perhaps defining event in the evolution of eukaryotic cells, he adds.

That’s because it seems clear that this organism’s ancestors had mitochondria that were then lost after the cells acquired their non-mitochondrial system for making iron-sulfur clusters.

Biology is amazing and mitochondria are one of the many amazing details. I wish so much that my education could have given biology a tiny fraction of the interest I have found it in after school.

Related: Human Gene Origins: 37% Bacterial, 35% Animal, 28% Eukaryotic – One Species’ Genome Discovered Inside Another’s – Parasite Evolved from Cnidarians (Jellyfish etc.) – Plants, Unikonts, Excavates and SARs

Parasite Evolved from Cnidarians (Jellyfish etc.)

Posted on November 22, 2015  Comments (0)

This is another instance of science research providing us interesting details about the very odd ways life has evolved on earth.

Genome sequencing confirms that myxozoans, a diverse group of microscopic parasites that infect invertebrate and vertebrate hosts, are actually highly reduced cnidarians — the phylum that includes jellyfish, corals and sea anemones.

“This is a remarkable case of extreme degeneration of an animal body plan,” said Paulyn Cartwright, associate professor of ecology and evolutionary biology at the University of Kansas (KU) and principal investigator on the research project. “First, we confirmed they’re cnidarians. Now we need to investigate how they got to be that way.”

images of myxozoans parasite spores and a jellyfish

Not only has the parasitic micro jellyfish evolved a stripped-down body plan of just a few cells, but via data generated at the KU Medical Center’s Genome Sequencing Facility researchers also found the myxozoan genome was drastically simplified.

“These were 20 to 40 times smaller than average jellyfish genomes,” Cartwright said. “It’s one of the smallest animal genomes ever reported. It only has about 20 million base pairs, whereas the average Cnidarian has over 300 million. These are tiny little genomes by comparison.”

Despite its radical phasedown of the modern jellyfish’s body structure and genome over millions of years, Myxozoa has retained the essential characteristic of the jellyfish — its stinger, or “nematocyst” — along with the genes needed to make it.

“Because they’re so weird, it’s difficult to imagine they were jellyfish,” she said. “They don’t have a mouth or a gut. They have just a few cells. But then they have this complex structure that looks just like stinging cell of cnidarian. Jellyfish tentacles are loaded with them — little firing weapons.”

The findings are the stuff of scientific fascination but also could have a commercial effect. Myxozoa commonly plague commercial fish stock such as trout and salmon.

“They’re a very diverse group of parasites, and some have been well-studied because they infect fish and can wreak havoc in aquaculture of economic importance,” Cartwright said.

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Cancer Rates Consistent Across Species Instead of Increasing Due to Body Mass

Posted on October 12, 2015  Comments (1)

It would seem sensible to think cancer should be more prevalent in species with a huge number of cells, and thus more cells to become cancerous. But cancer risk doesn’t increase in this way. This interesting, open source paper, sheds some light on what is behind this.

Solutions to Peto’s paradox revealed by mathematical modelling and cross-species cancer gene analysis

Whales have 1000-fold more cells than humans and mice have 1000-fold fewer; however, cancer risk across species does not increase with the number of somatic cells and the lifespan of the organism. This observation is known as Peto’s paradox. How much would evolution have to change the parameters of somatic evolution in order to equalize the cancer risk between species that differ by orders of magnitude in size? Analysis of previously published models of colorectal cancer suggests that a two- to three-fold decrease in the mutation rate or stem cell division rate is enough to reduce a whale’s cancer risk to that of a human. Similarly, the addition of one to two required tumour-suppressor gene mutations would also be sufficient.

We surveyed mammalian genomes and did not find a positive correlation of tumour-suppressor genes with increasing body mass and longevity. However, we found evidence of the amplification of TP53 in elephants, MAL in horses and FBXO31 in microbats, which might explain Peto’s paradox in those species. Exploring parameters that evolution may have fine-tuned in large, long-lived organisms will help guide future experiments to reveal the underlying biology responsible for Peto’s paradox and guide cancer prevention in humans.

Elephants in Kenya

Elephants in Kenya by John Hunter. See more photos from my trip to Kenya.

In another way it would make sense that large animals would have hugely increased risks of cancer. As they evolved, extremely high cancer rates would be a much bigger problem for them. Therefore it wouldn’t be surprising to find they have evolved a way of reducing cancer risks.

Despite these limitations, we found genes that have been dramatically amplified in specific mammalian genomes, the most interesting of which is the discovery of 12 TP53 copies in the genome of the African elephant. We subsequently cloned those genes and identified 19 distinct copies of TP53 in African elephants and 15–20 in Asian elephants [1]. Another potential lead for solving Peto’s paradox is MAL, which is found to have eight copies in the horse genome and two in microbat. This could be an example of convergent evolution where a large animal (horse) and a small, long-lived animal (microbat) both evolved extra copies of the same gene to overcome their increased risk of cancer. Further analysis and experimentation would need to be performed to determine the function of these copies and whether or not they provide enhanced suppression of carcinogenesis.

The researchers have found an interesting potential explanation for how that has been accomplished.

Related: The Only Known Cancerless Animal (the naked mole rat) – Webcast of a T-cell Killing a Cancerous Cell – Researchers Find Switch That Allows Cancer Cells to Spread – Cancer Vaccines

Defying Textbook Science, Study Finds Proteins Built Without DNA Instructions

Posted on January 3, 2015  Comments (2)

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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Epigenetics, Scientific Inquiry and Uncertainty

Posted on September 20, 2014  Comments (1)

Science is full of fascinating ideas. Epigenetics is one area I find particularly interesting. This previous post has a few links to learning more: DNA Passed to Descendants Changed by Your Life.

Angela Saini is one 109 people I follow on Twitter. I don’t see the point in “following” people on Twitter that you have no interest in, I only follow the small number of people that post Tweets I want to read.

In, Epigenetics: genes, environment and the generation game, Angela Saini looks at the confused state of current scientific understand now. It is very difficult to tell if, and if so, to what extent, epigenetic inheritance happens in people.

Professor Azim Surani, a leading developmental biologist and geneticist at the University of Cambridge, adds that while there is good evidence that epigenetic inheritance happens in plants and worms, mammals have very different biology. Surani’s lab carried out thorough studies on how epigenetic information was erased in developing mouse embryos and found that “surprisingly little gets through” the reprogramming process.

Professor Timothy Bestor, a geneticist at Columbia University in New York, is far more damning, claiming that the entire field has been grossly overhyped. “It’s an extremely fashionable topic right now. It’s very easy to get studies on transgenerational epigenetic inheritance published,” he says, adding that all this excitement has lowered critical standards.

Related: Epigenetic Effects on DNA from Living Conditions in Childhood Persist Well Into Middle Age – Medical Study Findings too Often Fail to Provide Us Useful Knowledge – Scientific Inquiry Process Finds That Komodo Dragons Don’t have a Toxic Bite After All

Continue reading →

DNA Contains Gene Control Instructions

Posted on December 19, 2013  Comments (0)

Scientists discover double meaning in genetic code

Scientists have discovered a second code hiding within DNA. This second code contains information that changes how scientists read the instructions contained in DNA and interpret mutations to make sense of health and disease.
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“For over 40 years we have assumed that DNA changes affecting the genetic code solely impact how proteins are made,” said Stamatoyannopoulos. “Now we know that this basic assumption about reading the human genome missed half of the picture. These new findings highlight that DNA is an incredibly powerful information storage device, which nature has fully exploited in unexpected ways.”

The genetic code uses a 64-letter alphabet called codons. The UW team discovered that some codons, which they called duons, can have two meanings, one related to protein sequence, and one related to gene control. These two meanings seem to have evolved in concert with each other. The gene control instructions appear to help stabilize certain beneficial features of proteins and how they are made.

The discovery of duons has major implications for how scientists and physicians interpret a patient’s genome and will open new doors to the diagnosis and treatment of disease.

“The fact that the genetic code can simultaneously write two kinds of information means that many DNA changes that appear to alter protein sequences may actually cause disease by disrupting gene control programs or even both mechanisms simultaneously,” said Stamatoyannopoulos.

The wonder of DNA continues to amaze.

Related: Epigenetic Effects on DNA from Living Conditions in Childhood Persist Well Into Middle Age – DNA Passed to Descendants Changed by Your Life – DNA based Algorithmic Self-Assembly

Go Slow with Genetically Modified Food

Posted on August 3, 2013  Comments (2)

My thoughts on Genetically Modified Organisms (GMO), specifically GM foods, basically boil down to:

  • messing with genes could create problems
  • we tend to (and especially those seeking to gain an advantage tend to – even if “we” overall wouldn’t the people in the position to take aggressive measures do) ignore risks until the problems are created (often huge costs at that point)
  • I think we should reduce risk and therefore make it hard to justify using GMO techniques
  • I agree occasionally we should do so, like it seems with oranges and bananas.
  • I agree the practice can be explained in a way that makes it seem like there is no (or nearly no) risk, I don’t trust we will always refrain from stepping into an area where there is a very bad result

Basically I would suggest being very cautious with GMO. I like science and technology but I think we often implement things poorly. I think we are not being cautious enough now, and should reduce the use of GMO to critical needs to society (patents on the practices need to be carefully studied and perhaps not permitted – the whole patent system is so broken now that it should be questioned at every turn).

Antibiotic misuse and massive overuse is an obvious example. We have doctors practicing completely unjustified misuse of antibiotics and harming society and we have factory farms massively overusing antibiotics causing society harm.

The way we casually use drugs is another example of our failure to sensibly manage risks, in my opinion. This of course is greatly pushed by those making money on getting us to use more drugs – drug companies and doctors paid by those companies. The right drugs are wonderful. But powerful drugs almost always have powerful side effects (at least in a significant number of people) and those risks are multiplied the more we take (due to interactions, weakness created by one being overwhelmed by the next etc.). We should be much more cautious but again we show evidence of failing to act cautiously which adds to my concern for using GMO.

I love antibiotics, but the way we are using them is endangering millions of lives (that is a bad thing). I don’t trust us to use science wisely and safely. We need to more consciously put barriers in place to prevent us creating massively problems.

Related: Research on Wheat Rust – The Avocado – Overfishing, another example of us failing to effectively cope with systemic consequences

Cell Aging and Limits Due to Telomeres

Posted on March 17, 2013  Comments (2)

When cells divide the process fails to copy DNA all the way to the end. Telomeres are are the end of DNA strands, as essentially a buffer of material that won’t cause information to be lost when part of the telomere isn’t copied. As DNA is copied, as new cells are created, the length of telomeres at the end is reduced. Once the telomeres are gone the cell will no longer divide.

The 2009 Nobel Prize in Physiology or Medicine went to 3 scientists for discovering how the chromosomes can be copied in a complete way during cell divisions and how they are protected against degradation. The Nobel Laureates have shown that the solution is to be found in the ends of the chromosomes – the telomeres – and in an enzyme that forms them – telomerase.

There is some debate over the benefit of the mechanism of cells not dividing do to lack of telomere. This can prevent cancerous cells from replicating (once they replicate to the extent that the necessary telomere buffer is gone). It is also seen that as telomeres get shorter the cells become more likely to become cancerous.

Cancer also can stimulate the production of telomerase which can stop telomeres from getting shorter as cells divide and thus allow the cancer cells to keep dividing (thus producing more cancer cell and increasing the amount of cancerous cells). Using telomerase to allow health cells to avoid the limits of division is being researched.

Are Telomeres the Key to Aging and Cancer? (University of Utah)

An enzyme named telomerase adds bases to the ends of telomeres. In young cells, telomerase keeps telomeres from wearing down too much. But as cells divide repeatedly, there is not enough telomerase, so the telomeres grow shorter and the cells age.
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Cells normally can divide only about 50 to 70 times, with telomeres getting progressively shorter until the cells become senescent, die or sustain genetic damage that can cause cancer.
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shorter telomeres are associated with shorter lives. Among people older than 60, those with shorter telomeres were three times more likely to die from heart disease and eight times more likely to die from infectious disease.

While telomere shortening has been linked to the aging process, it is not yet known whether shorter telomeres are just a sign of aging – like gray hair – or actually contribute to aging.

Related: The Naked Mole Rat is the Only Known Cancerless Animal – Webcast of a T-cell Killing a Cancerous Cell – RNA interference webcast

Evolution Follows a Predictable Genetic Pattern

Posted on November 1, 2012  Comments (0)

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.
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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 Ancestor – Cambrian Explosion Song – Bacteriophages: The Most Common Life-Like Form on Earth – Microcosm by Carl Zimmer

Key Indicator for Malignant Melanoma Found

Posted on September 20, 2012  Comments (2)

Skin cancer detection breakthrough

The researchers found that certain biochemical elements in the DNA of normal pigment-producing skin cells and benign mole cells are absent in melanoma cells. Loss of these methyl groups — known as 5-hmC — in skin cells serves as a key indicator for malignant melanoma. Loss corresponded to more-advanced stages of melanoma as well as clinical outcome.

Strikingly, researchers were able to reverse melanoma growth in preclinical studies. When the researchers introduced enzymes responsible for 5-hmC formation to melanoma cells lacking the biochemical element, they saw that the cells stopped growing.

“It is difficult to repair the mutations in the actual DNA sequence that are believed to cause cancer,” said Christine Lian, a physician-scientist in the Department of Pathology at BWH and one of the lead authors. “So having discovered that we can reverse tumor cell growth by potentially repairing a biochemical defect that exists — not within the sequence but just outside of it on the DNA structure — provides a promising new melanoma treatment approach for the medical community to explore.”

Because cancer is traditionally regarded as a genetic disease involving permanent defects that directly affect the DNA sequence, this new finding of a potentially reversible abnormality that surrounds the DNA (thus termed “epigenetic”) is a hot topic in cancer research, according to the researchers.

In the United States, melanoma is the fifth most common type of new cancer diagnosis in men and the seventh most common type in women. The National Cancer Institute estimates that in 2012 there will be 76,250 new cases and 9,180 deaths in the United States owing to melanoma.

Thankfully scientists keep making great progress in understanding and finding potential clues to treating cancer. And big gains have been made in treating some cancers over the last few decades. But the research successes remain difficult to turn into effective solutions in treating patients.

I am thankful we have so many scientists doing good work in this difficult and important area (cancer).

Related: Webcast of a T-cell Killing a Cancerous Cell – Nanoparticles With Scorpion Venom Slow Cancer Spread – DNA Passed to Descendants Changed by Your Life – Researchers Find Switch That Allows Cancer Cells to Spread