Posts about genes

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

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 AgeAmazing Designs of LifeOne Species’ Genome Discovered Inside Another SpeciesBdelloid Rotifers Abandoned Sex 100 Million Years Ago

All present-day Life on Earth Has A Single Ancestor

All present-day life arose from a single ancestor

All life on Earth shares a single common ancestor, a new statistical analysis confirms.

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.

A universal common ancestor is at least 102,860 times more probable than having multiple ancestors, Theobald calculates.

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 LifeEvolution is Fundamental to ScienceBacteria “Feed” on Earth’s Ocean-Bottom Crust

A Breakthrough Cure for Ebola

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.

Related: Science Explained: RNA InterferenceAmazing Science: RetrovirusesEbola Outbreak in Uganda (Dec 2007)

Essentials of Genetics Website Reference

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 EvolutionDNA Passed to Descendants Changed by Your LifeAnger at Anti-Open Access Press Strategy

What Dogs Reveal About Evolution

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.

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.

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.

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 CatsDarwin’s Beetles Still Producing SurprisesBackyard Wildlife: Fox

Microcosm by Carl Zimmer

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 EarthForeign Cells Outnumber Human Cells in Our BodiesAmazing Designs of LifeAmazing Science: RetrovirusesOne Species’ Genome Discovered Inside Another’s

Science Explained: RNA Interference

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.

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 VirusesPosts explaining scientific principles and conceptsDNA Passed to Descendants Changed by Your LifeWhy Does Hair Turn Grey as We Age?Amazing Science: Retroviruses

The Only Known Cancerless Animal

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 Spreadposts on university researchGene Duplication and EvolutionGlobal Cancer Deaths to Double by 2030
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Antigen Shift in Influenza Viruses

Antigenic shift is the process by which at least two different strains of a virus, (or different viruses), especially influenza, combine to form a new subtype having a mixture of the surface antigens of the two original strains.

Pigs can be infected with human, avian and swine influenza viruses. Because pigs are susceptible to all three they can be a breeding ground for antigenic shift (as in the recent case of H1N1 Flu – Swine Flu) allowing viruses to mix and create a new virus.

Related: Swine Flu: a Quick OverviewOne Sneeze, 150 Colds for CommutersWashing Hands Works Better than Flu Shots (study results)Learning How Viruses Evade the Immune SystemAlligator Blood Provides Strong Resistance to Bacteria and Viruses

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Resurrection of the Human IRGM Gene

Interesting open access paper on Death and Resurrection of the Human IRGM Gene. Author summary:

The IRG gene family plays an important role in defense against intracellular bacteria, and genome-wide association studies have implicated structural variants of the single-copy human IRGM locus as a risk factor for Crohn’s disease. We reconstruct the evolutionary history of this region among primates and show that the ancestral tandem gene family contracted to a single pseudogene within the ancestral lineage of apes and monkeys.

Phylogenetic analyses support a model where the gene has been “dead” for at least 25 million years of human primate evolution but whose ORF became restored in all human and great ape lineages. We suggest that the rebirth or restoration of the gene coincided with the insertion of an endogenous retrovirus, which now serves as the functional promoter driving human gene expression. We suggest that either the gene is not functional in humans or this represents one of the first documented examples of gene death and rebirth.

Related: 8 Percent of the Human Genome is Old Virus GenesOld Viruses Resurrected Through DNAOne Species’ Genome Discovered Inside Another’sposts on genesGene against bacterial attack unravelledGene Duplication and Evolution

Simple Webcasts on Evolution and Genes

Webcast from 23andme on human evolution. Continued: What are genes?, What are SNPs? (Single Nucleotide Polymorphisms), Where do your genes come from? and What is phenotype?. These webcasts provide an easy to understand overview. Sergey Brin, Google co-founder and husband of 23andme co-founder Anne Wojcicki. People have 23 pairs of chromosomes.

What are SNPs?:

For a variation to be considered a SNP, it must occur in at least 1% of the population. SNPs, which make up about 90% of all human genetic variation, occur every 100 to 300 bases along the 3-billion-base human genome.

SNPs do not cause disease, but they can help determine the likelihood that someone will develop a particular illness. One of the genes associated with Alzheimer’s disease, apolipoprotein E or ApoE, is a good example of how SNPs affect disease development. ApoE contains two SNPs that result in three possible alleles for this gene: E2, E3, and E4. Each allele differs by one DNA base, and the protein product of each gene differs by one amino acid.

Related: Understanding the Evolution of Human Beings by CountryEvolution is Fundamental to Science8 Percent of the Human Genome is Old Virus Genesscience webcasts

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