Mighty mice meet their match

by Tyler Shendruk

Published: Feb 17

The problem
IT’S AN EVOLUTIONARY arms race out there. Viruses that infect organisms evolve to evade the immune systems of their hosts. Every time that happens, host animals like us must create strategies to battle the infections and diseases they cause.
For example, retroviruses are a family of viruses that have an RNA genome. While it’s often said that the fundamental building block of life is DNA, the genetic material of these viruses is RNA. Retroviruses produce DNA from their RNA and insert it into a host’s genome, changing the host forever. From then on, the virus replicates with the host cell’s DNA.
Our immune system protects us against most retroviruses. Only the human immunodeficiency virus (HIV) and the human T-lymphotropic virus (HTVL) have been shown to cause diseases in humans. Both have evolved ways to get around our immune defences.

The researcher
Marc-Andre Langlois does his research for the Faculty of Medicine at Roger Guindon Hall on the General Hospital Campus. He studies how retroviruses replicate and infect cells—specifically how cells are able to protect themselves against retroviruses.

The project
One of the best armaments our cells have is a family of proteins called APOBEC3. It’s still a mystery how they do it, but APOBEC3 proteins can completely deactivate all retroviral invaders by mutating the attacking DNA before it can be inserted into the host’s genome. The exceptions are HIV and HTVL. Those two have out evolved our protein parapets.
While primates have seven APOBEC3 proteins, mice have only one. This really interests Langlois. The mice APOBEC3 protein is more general than any of our seven. However, even mice can be infected by retroviruses. One of their versions of HIV is called AKV.

The key
Langlois was able to observe the arms race between AKV and the mouse APOBEC3 protein. Mice with diverse abundances of APOBEC3 were better at restricting AKV than mice with any specific form of APOBEC3. They can mutate (and so deactivate) more variations of the retrovirus. Langlois concludes that, since APOBEC3 stops infections by mutating the attackers, it pressures AKV to evolve. Because the mice’s own weapons against AKV cause it to mutate at an exaggerated rate, a broad set of deterrents provides for the best defense against such a varied viral foe.

Miniscule monsters

by Tyler Shendruk

Published: Feb 9

The problem
Genomicists have a serious bias toward “model” organisms. Model organisms are species that have historically been well studied. Fruit flies, yeast, zebrafish, and mice are examples of model organisms. So are humans.
But these model organisms are each just some leaf on a random twig of the tree of life. Scientists are only beginning to realize the true extent of biodiversity and the staggering variety of differing genes and structures that make up genomes.

The researcher
Nicolas Corradi studies comparative genomics, which means that he sequences organisms’ genomes and then compares their genes and structure to those of other species. Corradi’s lab in the biology department at the University of Ottawa focuses on unicellular eukaryotes, single-celled micro-organisms that harbour curious genomes in their nuclei.

The project
Corradi’s favourite eukaryotes are microsporidia, parasitic unicellular fungi. These little monsters are highly adapted for infecting host cells. They are opportunistic bugs that steal everything they need to survive from their host. In fact, the only time microsporidia spend outside of a host cell is as spores, scouring to invade other cells.

The key
Corradi sequenced the genome of the microsporidia Encephalitozoon intestinalis. This particular microsporidia has the smallest nuclear genome of any known organism. It is made of only 1,800 genes (1,500 times smaller than the human genome and 20 per cent smaller than the next smallest genome ever sequenced).
Why do they have such small genomes? Because these microsporidia are marauding picaroons. They don’t do anything they don’t have to. They steal so much from their hosts that they have shed every gene but the bare minimum needed to function.
Evolutionarily speaking, it is easier to lose genes than to gain them, so these microsporidia are extremely adapted for their parasitic lifestyle. Their genome is so compact that Corradi believes it may represent the limit for a fully functional genome.

Digital drugs

by Tyler Shendruk

Published: Feb 2

The problem
IT IS POSSIBLE to cure certain cancers by surgically removing the tumors, but this requires that every single cancer cell is extracted. If any cancer cells remain, or if they spread to further, undetected sites, only remission has been achieved—not a complete cure.
Therefore, tracking surviving cancer cells is vitally important. Given the opportunity, they will grow into deadly new tumors. Unfortunately, treatments that can deal with remaining cells, like radiation or chemotherapy, indiscriminately kill cancer cells and healthy cells alike, making the treatments brutal on the body. Targeted therapies are at the forefront of cancer treatment.

The researcher
In the Department of Chemistry, professor Maxim Berezovski has a laboratory that is, in many ways, obsessed with selectivity. In one project, Berezovski studies separation techniques that can teach him about biochemical reaction rates. In another, he isolates biomarkers from cells. In yet another, he marks cells of one type without marking any of the others. The flags he uses to mark cells are called aptamers.

The project
Aptamers are short polymers of nucleic acids that bind to specifically targeted molecules. In many ways, researchers can use them as synthetic artificial antibodies. Berezovski builds them from little chunks of DNA to target the surface of different cells, in particular cancer cells. The selectivity of aptamers makes them perfect for marking or attacking cancer cells while ignoring the healthy ones.

The key
Berezovski proposes that once a tumor is surgically removed, a cocktail of aptamers can be specifically designed for those individual tumor cells. Tumors that reappear are actually clones of the original tumor. This means that the personal recipe of aptamers for the original tumor could be kept as a digital record in case of recurrence. Since there is no need to keep the actual aptamers, Berezovski refers to this record as a digital drug.
The digital drug could be used to produce a personalized mixture of aptamers that will target clones of the original tumor. Doctors could then attach labels to the aptamers to track cancer cells that escaped surgical removal or to identify new tumors. The selectivity of aptamers could even direct the delivery of toxins or medicine specifically to the tumor, allowing for a more finite cancer survival rate.

Shut up, Science

The impact of censorship in science research on our democracy

by Tyler Shendruk

Published: Feb 2

FREEDOM OF EXPRESSION is the root of the twins of Enlightenment: Science and Democracy. The essence of science is the freedom to question any dogma, the freedom to discover truth. And that right to question lies at the core of democracy. Without the freedom to exchange information among all people, how can political debate in a democracy have any hope? It’s impossible to overstate the importance of the dissemination of information and the right to free enquiry of our political system.
And yet, Canadians sanction the censorship of science by their silence. Before we look in the mirror, let’s talk about our neighbours. Five years ago, James Hansen, the head of NASA’s institute on planetary science, accused NASA public relations staff of suppressing his public statements on the causes of climate change. It became clear that the political appointee who tried to silence Hansen’s findings was following orders to ensure that scientists’ communication with the press was in line with the official stance of the White House.
Hansen’s experience with scientific censorship wasn’t an isolated case. Nearly half of federal climate scientists in the U.S. claim that they have been pressured to remove the words “global warming” or “climate change” from their reports. They claim their work has been edited by bureaucrats, and many said they too have been prevented from talking to the media. More recently—and despite a new government that has promised to “restore science to its rightful place”—federal scientist talking about the BP oil spill have required government clearance before speaking to the press about their findings.
Bad Americans.
Oh wait—things may sound bad in the United States, but here in Canada the situation is even worse. In this country, politics always trump science.
Stephen Harper’s Conservative government is all about message control—both within the Conservative party and also for federal employees. In 2007, Environment Canada implemented a new federal communications policy that demanded that federal scientists obtain permission from the federal government prior to giving any interviews. The regulation is reminiscent of the Bush administration’s attitudes toward scientific debate, but is far more institutionalized and overarching. By ignoring or denying interview requests, the government steals the ability of the country’s news outlets to talk to experts and cover scientific findings.
Effectively, the Conservative Party has complete control over media coverage on climate science. Since the Harper government introduced the new rules, media coverage of climate science dropped by more than 80 per cent. It seems that when the conclusions of the Canadian government’s own climate research run counter to the Conservative government’s stance on the Kyoto Protocol, the oil sands, or any of the party’s policies toward the environment, potential debate is simply squelched.
After the loss of the mandatory long-form census, the Professional Institute of the Public Service of Canada, a union for federal scientists, launched a campaign against Canada’s “worrying trend away from evidence-based policy-making.” Canadian scientists have begun to fight back, but federally employed climate scientists remain gagged.
Environment Minister Jim Prentice’s campaign of soft censorship through reduced funding to independent research is also an attack that can’t be ignored. In theory, agencies like the Canadian Foundation for Climate and Atmospheric Science fund university-based research independently from political bodies, but last year Prentice threatened these investments. Without money to conduct research, scientists can’t provide the public with evidence informing debate.
The people of Canada pay taxes to fund scientific research, but the government of Canada doesn’t let us hear the results. Scientists get public funding to research questions that have serious ramifications in modern political debate. We must demand that they get the chance to report back to Canadians with accuracy—otherwise it amounts to a conscious effort on the part of the government to keep the Canadian voters uninformed about the consequences of federal policies.

(Almost) everything you ever needed to know about isotopes

By Tyler Shendruk

Published: Feb 2 (for X-ray isotopes trump nuclear)

Atoms aren’t unchanging blocks of matter. Let me tell you, it’s nearly impossible to figure out where an electron is at any given moment. And the nucleus! Nuclei are constantly jumping from one energy state to another as protons and neutrons push and pull, sometimes absorbing energy and sometimes ejecting it. Every once in a while, they decay and become something else entirely. Nuclei are constantly hopping down the periodic table.

So it’s not surprising that the number of neutrons in a nucleus isn’t always the same as the number of protons. Oxygen isn’t just oxygen—it’s any atom with eight protons. The number of neutrons can be anything from 4 to 20! Atoms with the same number of protons are called isotopes: it doesn’t matter how many neutrons there are. The exceeding majority of isotopes aren’t stable. Some decay radioactively and their radiation can be used for all kinds of great scientific and medical purposes.