#10 Resurrecting Coffee, Predators Mitigating the Climate and Turning off Mitochondria...
The resurrecting of a coffee-destroying fungus, the mitigating effect of predators on climate change and pathogens turning off mitochondrial defences.
☕Resurrecting Coffee?
Resurrecting a coffee-destroying fungus to Study It…
A fungal species named Fusarium xylarioides was recently awoken from the dead in the aim to better understand modern day populations. The Centre for Agriculture and Biosciences International (CABI) holds cryogenic freezers with around 30,000 strains of living microorganisms. This preserves strains and species, allowing scientists to “go back in time” to study fungal evolution. Freezing the Fusarium xylarioides species, meant that Imperial College London graduate Lily Peck, could not only better understand the history of the fungal disease in coffee plants - but perhaps identify new and innovative ways to protect against it.
This particular species causes coffee wilt disease in crops in Ethiopia as well as other African countries. It was first detected in the 1920s, with the fungus drying out leaves, restricting water transport and eventually killing the plant. An international collaboration to reduce the spread temporarily brought the endemic pathogen under control with improved crop breeding and hygiene. However, in the 1970s the species re-emerged. Since, two clear populations have evolved, one based on Arabica coffee in Ethiopia with the other on Robusta coffee in the Congo basin.
To have a better understanding of how the fungus had changed over the past few decades, Peck and her team rehydrated the samples with water to reawaken a total of 6 pre 1970 strains. These 6 strains were responsible for outbreaks of coffee wilt disease and named Coffea after the host plant’s genus. Following Peck checking fungal spores for contamination, DNA was extracted and sequenced.
The data showed that the robusta-infecting F. xylarioides hold strong genetic similarities to the preserved Coffea stains. This therefore suggests that the robusta population, emerged from a wider recombining population of Coffea strains from the initial pre-1970s outbreak. Peck went on to say that, “the arabica population appears to have diverged separately and shares a common ancestor with both the Coffea and the robusta strains” of F. xylarioides.
The research teams findings show that the two current day populations are genetically distinct. The research also found that both the modern F. xylarioides strains share genes with a fungal strain named F. oxysporum. Interestingly this is a fungal strain that causes wilting in banana trees. These are often interplanted with the coffee crops. Peck went on to say that understanding the genetics of disease-causing strains could be useful to coffee cultivators. Different fungal pathogens often rely on similar genes to bypass plant defences. Being able to identify the genes and the expression patterns of the genes may lead to innovative and novel solutions to combat the malignant fungal infections.
Morgan Carter, postdoc at the University of Arizona who specialises in plant associated bacterial-fungal interactions noted that the study used short-read sequencing to complete their research. Long-read sequencing could provide a clearer picture of which genetic elements led to the fungal evolution and resultantly provide a solution to the issue.
Peck is now studying the gene expression of half century old F. xylarioides strains as they infect coffee plants in a controlled environment at Imperial. Peck stated that “We can use this approach to study historic emergence of disease for lots of different cases,” adding that she is keen to better understand the differences between the robusta and arabica fungus types.
☀️Predators Help Buffer Climate Change?
Predators help buffer the effects of climate change on biodiversity…
Scientists from Trinity College Dublin and Hokkaido University suggest that predator species may buffer against some of the negative affects of climate change, mitigating the loss of biodiversity. The team emphasise the importance of conserving biodiversity, specifically top predators, highlighting the potential for species extinction to worsen the effects of climate change.
Through assembling communities of freshwater organisms in experimental streams at a location in Northern Japan, the team would be able to record data on varied environmental conditions. The stream communities were exposed to realistic heatwaves, with some sample streams including a dominant predator. This being the Sculpin fish (Cottoidea).
The predominant discovery was that the artificial heatwaves destabilised the algal communities in the streams. This meant that the differences and biodiversity found within them disappeared, as they resembled each other more closely. However, this resultant loss in biodiversity only occurred in sample sites where the predator sculpin fish was absent from the community. The sites with the predator represented a more expected level of biodiversity in comparison to the sites where they were absent.
Algal communities are a cornerstone of many ecosystems, being one of the fundamental species that other organisms rely upon. Therefore a loss of algal biodiversity can trigger positive feedback loops throughout the ecosystem. Furthermore, scientists only discovered that important heatwave effects such as total agal biomass change, only occurred once the heatwave had passed, representative of how some of the catastrophic events triggered by climate change, may be delayed.
Dr Samuel Ross, who led the experiment in Japan, stated that “We found that predator extinctions can interact with heatwaves to further undermine the stability of ecosystems. This highlights how the climate and biodiversity crises are completely intertwined, really just two sides of the same coin.” Furthermore, the data shows how the ecological consequences of heatwaves can amplify over time as their impacts propagate throughout ecosystems and communities.
🦠Pathogens Turn Off Mitochondria?
Pathogens turn off mitochondrial defences…
Mitochondria are organelles found in large numbers of most cells, key to numerous biochemical processes such as respiration and energy production. Whilst they are predominantly known as energy suppliers for our cell, they also play an important role in the defence against pathogens. They can initiate an immune response as well as depriving pathogens of the nutrients needed to grow. A research team from the Max Planck Institute for Biology of Ageing in Cologne, Germany, led by Lena Pernas, has show that pathogens may have the ability to “turn off” mitochondrial defensive mechanisms by hijacking a normal cellular response to stress.
Pathogens obtain nutrients from their host cells in order to survive and counter the defences of the host. One of these defences being the mitochondria who can deprive them of needed nutrients that allow the pathogen to grow. The research team set out to find how the mitochondrial behaviour changes when mitochondria and pathogens meet in cells. Due to the outer membrane of these organelles, being the first contact point of pathogens, a focus was placed on the research of the membrane itself.
The researchers first infected the cells with a parasite named Toxoplasma gondii, which is a parasite linked to humans. When the team observed, live under the microscope, what happens to the outer compartment of mitochondria, they observed that the mitochondria “shed their skin”. The mitochondria was seen to be shedding large structure from their outer membrane when in contact with the parasite. This raised questions as to why, the mitochondria, would lose the protection between the parasite and the rest of the cell…
The research team was able to show that the pathogen has a “trick” protein that functionally mimics a host mitochondrial protein. By binding to the receptor located on the outer membrane of the mitochondria, the parasite gains access to machinery that ensures proteins are transported inside the mitochondria. "In doing so, the parasite hijacks a normal host response to mitochondrial stress that, in the context of infection, effectively disarms the mitochondria" Pernas said. Furthermore other researchers have shown that a SARS CoV 2 virus protein is also capable of binding to the transport receptor. Therefore, the receptor is shown to play an important role in the host pathogen interaction. However further investigation is needed to fully understand the its role during infections…
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🔬 Evolution
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📷 Weekly Camera Roll
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🔗Reference List
☕Resurrecting Coffee?
The Scientist/ Chloe Tenn. (2022) Researchers Resurrect Coffee-Destroying Fungus—to Study It. https://www.the-scientist.com/notebook/researchers-resurrect-coffee-destroying-fungus-to-study-it-69526
☀️Predators Help Buffer Climate Change?
Trinity College Dublin. "Predator species help to buffer climate change impacts on biodiversity." ScienceDaily. ScienceDaily, 12 January 2022. <www.sciencedaily.com/releases/2022/01/220112121553.htm>.
Ross, Samuel & Molinos, Jorge & Okuda, Atsushi & Johnstone, Jackson & Atsumi, Keisuke & Futamura, Ryo & Williams, Maureen & Matsuoka, Yuichi & Uchida, Jiro & Kumikawa, Shoji & Sugiyama, Hiroshi & Kishida, Osamu & Donohue, Ian. (2021). Predators mitigate the destabilising effects of heatwaves on multitrophic stream communities. Global Change Biology. 28. 10.1111/gcb.15956.
🦠Pathogens Turn Off Mitochondria?
Max Planck Society. (2022) How pathogens can turn off mitochondrial defence mechanisms. https://phys.org/news/2022-01-pathogens-mitochondrial-defense-mechanisms.html
Xianhe Li et al, Mitochondria shed their outer membrane in response to infection-induced stress, Science (2022). DOI: 10.1126/science.abi4343. www.science.org/doi/10.1126/science.abi4343