The collaborative study from the University of British Columbia (UBC) and the Strategic Salmon Health Initiative (SSHI) — a partnership between Fisheries and Oceans Canada (DFO), Genome BC and the Pacific Salmon Foundation — traces the origins of PRV to Atlantic salmon farms in Norway and finds that the virus is now almost ubiquitous in salmon farms in B.C.

It also shows that wild Chinook salmon are more likely to be infected with PRV the closer they are to salmon farms, which suggests farms transfer the virus to wild salmon.

Genome sequencing of viruses from farms and wild fish further indicates that transmission occurs between farms and wild salmon.

“Both our genomic and epidemiological methods independently came to the same conclusion, that salmon farms act as a source and amplifier of PRV transmission,” said Dr. Gideon Mordecai, a viral ecologist and Liber Ero fellow with UBC Science and researcher with UBC Medicine, who led the study. “Because separate lines of independent evidence all point to the same answer, we’re confident in our finding.”

Sequencing of 86 PRV genomes helped researchers track the history of PRV emergence in British Columbia. They estimate that the lineage of PRV in the North East Pacific diverged from PRV in the Atlantic Ocean approximately 30 years ago. This suggests that the introduction of PRV to B.C. and infection of wild Pacific salmon is a relatively recent phenomenon, coincident with the growth of salmon aquaculture in the province — not dating back to early attempts to introduce Atlantic salmon to the region, starting in 1874.

“There is much confusion about where PRV is originally from, whether it is transmitted between farmed and wild salmon, and how different lineages of the virus cause different severities of disease,” said Dr. Mordecai. “This study’s genome sequencing clearly indicates PRV is not native to B.C. waters — it originated in the Atlantic Ocean and has been spread around the world through salmon aquaculture.”

The study highlights the role of aquaculture in introducing novel pathogens to new regions, where they then spread to wild fish, and integrates the expertise of the two senior authors, Dr. Kristi Miller, a DFO scientist and Professor Jeffrey Joy, a UBC evolutionary geneticist. It demonstrates the value of genomics in the surveillance of viral pathogens affecting important fisheries resources and how analytical methods derived from the epidemiology of human viruses can be adapted and applied to conserving wild salmon populations.

Further analysis of PRV genomes generated by the study suggested that there has been a growth in the number of PRV infections in B.C. over recent decades. This finding corresponds with the regional growth in salmon aquaculture and high rates of viral infection in salmon farms.

“Our finding that PRV is transmitted between farmed and wild salmon is particularly relevant given recent field and laboratory studies showing the lineage of PRV in B.C. is likely to cause disease in both Pacific and Atlantic salmon” says Dr. Mordecai. A recent Norwegian study found that a Canadian isolate of the virus causes heart lesions in Atlantic salmon. More importantly to the Pacific ecosystem, PRV has been associated with a different disease in Chinook salmon in which blood cells rupture, leading to kidney and liver damage. These are in contrast to the DFO’s assessment that PRV is not a disease agent.

“Our study reaffirms that a more precautionary approach to managing salmon farming in BC is warranted,” says study co-author Dr. Andrew Bateman, of the Pacific Salmon Foundation. “The PRV findings, in particular, support calls to transition from open-net salmon farming towards farming technology that doesn’t allow disease transfer between farmed and wild salmon, protecting BC’s wild Pacific salmon from serious risk in the process.”

“The study provides foundational information necessary to assess the risk of salmon aquaculture on wild fish, as recommended by the Auditor General of Canada’s 2018 Report on Salmon Farming, which criticized DFO’s ability to manage aquaculture in a precautionary manner,” says Professor Jeffrey Hutchings of Dalhousie University, a leading Canadian fisheries scientist who was not involved with the research. “The work by Mordecai, Miller, and colleagues on PRV provides the most compelling, scientifically objective evidence to date that wild salmon in BC are at increased risk of disease because of open net-pen Atlantic salmon aquaculture,” adds Professor Hutchings.

Perovskites have drawn attention over the past decade because of their ability to act as semiconductors even when there are defects in the material’s crystal structure. This makes perovskites special because getting most other semiconductors to work well requires stringent and costly manufacturing techniques to produce crystals that are as defect-free as possible. In what amounts to the discovery of a new state of matter, the McGill team has made a step forward in unlocking the mystery of how perovskites pull off this trick.

“Historically, people have been using bulk semiconductors that are perfect crystals. And now, all of a sudden, this imperfect, soft crystal starts to work for semiconductor applications, from photovoltaics to LEDs,” explains senior author Patanjali Kambhampati, an associate professor in the Department of Chemistry at McGill. “That’s the starting point for our research: how can something that’s defective work in a perfect way?”

Quantum dots, but not as we know them

In a paper published May 26 in Physical Review Research, the researchers reveal that a phenomenon known as quantum confinement occurs within bulk perovskite crystals. Until now, quantum confinement had only been observed in particles a few nanometres in size — the quantum dots of flatscreen TV fame being one much-vaunted example. When particles are this small, their physical dimensions constrain the movement of electrons in a way that gives the particles distinctly different properties from larger pieces of the same material — properties that can be fine-tuned to produce useful effects such as the emission of light in precise colours.

Using a technique known as state-resolved pump/probe spectroscopy, the researchers have shown a similar type of confinement occurs in bulk caesium lead bromide perovskite crystals. In other words, their experiments have uncovered quantum dot-like behaviour taking place in pieces of perovskite significantly larger than quantum dots.

Surprising result leads to unexpected discovery

The work builds on earlier research which established that perovskites, while appearing to be a solid substance to the naked eye, have certain characteristics more commonly associated with liquids. At the heart of this liquid-solid duality is an atomic lattice able to distort in response to the presence of free electrons. Kambhampati draws a comparison to a trampoline absorbing the impact of a rock thrown into its centre. Just as the trampoline will eventually bring the rock to a standstill, the distortion of the perovskite crystal lattice — a phenomenon known as polaron formation — is understood to have a stabilizing effect on the electron.

While the trampoline analogy would suggest a gradual dissipation of energy consistent with a system moving from an excited state back to a more stable one, the pump/probe spectroscopy data in fact revealed the opposite. To the researchers’ surprise, their measurements showed an overall increase in energy in the aftermath of polaron formation.

“The fact that the energy was raised shows a new quantum mechanical effect, quantum confinement like a quantum dot,” Kambhampati says, explaining that, at the size scale of electrons, the rock in the trampoline is an exciton, the bound pairing of an electron with the space it leaves behind when it is in an excited state.

“What the polaron does is confine everything into a spatially well-defined area. One of the things our group was able to show is that the polaron mixes with an exciton to form what looks like a quantum dot. In a sense, it’s like a liquid quantum dot, which is something we call a quantum drop. We hope that exploring the behavior of these quantum drops will give rise to a better understanding of how to engineer defect-tolerant optoelectronic materials.”

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The team found that historic and ongoing evolution are widespread across the devils’ genome, but there is little overlap of genes between those two timescales. These findings, published in Proceedings of the Royal Society B, suggest that if transmissible cancers occurred historically in devils, they imposed natural selection on different sets of genes.

Tasmanian devils suffer from a transmissible cancer called devil facial tumor disease (DFTD). Unlike typical cancers, tumor cells from transmissible cancers are directly transferred from one individual to another like an infectious disease. DTFD is most commonly transmitted from host to host as devils bite each other during mating season. The tumors become malignant and can kill their hosts within six months.

DFTD was first discovered in 1996, and the recent discovery of a second transmissible cancer in Tasmanian devils in 2016 suggests that they may be prone to this unique type of disease. The threat of these two cancers has prompted conservation efforts.

“For the conservation of Tasmanian devils, our work adds to the growing list of genes that we have observed to be evolving in response to DFTD,” said Paul Hohenlohe, U of I Department of Biological Sciences associate professor, Institute for Bioinformatics and Evolutionary Studies (IBEST) principal investigator and senior author on the paper. “We can monitor genetic diversity of these genes in wild populations to understand whether and how these populations can adapt and survive in the face of DFTD.”

Using genomic sequencing and data analysis, the research team tested for natural selection in Tasmanian devils in response to DFTD to find out whether they are evolving as a result of the disease. They also looked for evidence of natural selection in the devils’ evolutionary history to test whether the genes that are evolving under DFTD show evidence of historical natural selection.

Finding little overlap in what genes are involved at historical and modern timescales, the team determined that if transmissible cancers have occurred historically in devils, they caused natural selection on different sets of genes. Their results and analysis of historical selection suggest that DFTD is a newly emerging selective force that distinctly shapes today’s wild devils.

This information can be used to inform conservation efforts by identifying targets for genetic monitoring and guiding maintenance of adaptive potential in Tasmanian devil populations.

“Our work suggests that maintaining genetic diversity across a wide set of functionally important genes is critical to make sure Tasmanian devils are able to adapt to transmissible cancers and other threats to their survival,” Hohenlohe said.

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In a study published on May 25, 2021, in Nature Communications, the investigators showed that using these compounds increased the regeneration of muscle cells in mice by activating the precursors of muscle cells, called myogenic progenitors. Although more work is needed before this approach can be applied in humans, the research provides insight into the underlying mechanisms related to muscle regeneration and growth and could one day help athletes as well as aging adults regenerate tissue more effectively.

“Loss of these progenitors has been connected to age-related muscle degeneration,” says Salk Professor Juan Carlos Izpisua Belmonte, the paper’s senior author. “Our study uncovers specific factors that are able to accelerate muscle regeneration, as well as revealing the mechanism by which this occurred.”

The compounds used in the study are often called Yamanaka factors after the Japanese scientist who discovered them. Yamanaka factors are a combination of proteins (called transcription factors) that control how DNA is copied for translation into other proteins. In lab research, they are used to convert specialized cells, like skin cells, into more stem-cell-like cells that are pluripotent, which means they have the ability to become many different types of cells.

“Our laboratory previously showed that these factors can rejuvenate cells and promote tissue regeneration in live animals,” says first author Chao Wang, a postdoctoral fellow in the Izpisua Belmonte lab. “But how this happens was not previously known.”

Muscle regeneration is mediated by muscle stem cells, also called satellite cells. Satellite cells are located in a niche between a layer of connective tissue (basal lamina) and muscle fibers (myofibers). In this study, the team used two different mouse models to pinpoint the muscle stem-cell-specific or niche-specific changes following addition of Yamanaka factors. They focused on younger mice to study the effects of the factors independent of age.

In the myofiber-specific model, they found that adding the Yamanaka factors accelerated muscle regeneration in mice by reducing the levels of a protein called Wnt4 in the niche, which in turn activated the satellite cells. By contrast, in the satellite-cell-specific model, Yamanaka factors did not activate satellite cells and did not improve muscle regeneration, suggesting that Wnt4 plays a vital role in muscle regeneration.

According to Izpisua Belmonte, who holds the Roger Guillemin Chair, the observations from this study could eventually lead to new treatments by targeting Wnt4.

“Our laboratory has recently developed novel gene-editing technologies that could be used to accelerate muscle recovery after injury and improve muscle function,” he says. “We could potentially use this technology to either directly reduce Wnt4 levels in skeletal muscle or to block the communication between Wnt4 and muscle stem cells.”

The investigators are also studying other ways to rejuvenate cells, including using mRNA and genetic engineering. These techniques could eventually lead to new approaches to boost tissue and organ regeneration.

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