Category Archives: Transhuman News

In just over 75 years, DNA deoxyribonucleic acid has risen in public and scientific status from being an obscure molecule with presumed accessory or structural functions inside the nucleus, to the icon of modern bioscience.

So wrote Ralf Dahm, Director of Scientific Management at Germanys Institute of Molecular Biology, in the journal Developmental Biology in 2005.

The DNA story may appear to begin in 1944, Rahm adds, with crucial discoveries by researchers Oswald Avery, Colin MacLeod and Maclyn McCarty. But it really began back in 1869, with the young Swiss physician Johann Friedrich Miescher.

McCarty, an American, and Canadians Avery and MacLeod were working at Rockefeller University in New York when they discovered that DNA, not proteins, had the ability to transform the properties of cells.

An article published by the US National Human Genome Research Institute says biochemists had previously assumed that deoxyribonucleic acid was a relatively unimportant, structural chemical in chromosomes and that proteins, with their greater chemical complexity, transmitted genetic traits.

Avery, MacLeod and McCarty were studying Streptococcus pneumoniae bacteria that can cause pneumonia. They wanted to discover how a non-virulent strain could be transformed into a virulent form and to understand its chemical nature.

In 1944 they identified and isolated DNA as the transforming principle. This was the agent that could produce an enduring, heritable change in an organism.

Within 10 years of these experiments, Dahm says, James Watson and Francis Crick deciphered its structure and, yet another decade on, the genetic code was cracked.

But it would not have been possible without Miescher.

Born in Basel on 13 August 1844, he studied medicine, like his father and an uncle before him, receiving his qualification in 1868. But severe ear infections left him with impaired hearing and, believing this would hinder his ability to work as a doctor, he turned to a career in chemistry and medical research.

He went to work at the University of Tubingen in Germany, in a newly established faculty of natural science, tasked with researching the chemical composition of leukocytes, or white blood cells.

To obtain material, he would collect freshly used surgical bandages from a nearby hospital, wash off the pus and filter out the leukocytes.

Dahm, writing in the journal Human Genetics, says that in his experiments Miescher noticed a precipitate of an unknown substance, which he characterised further.

Analyses of its elementary composition revealed that, unlike proteins, it contained large amounts of phosphorous and lacked sulphur. Miescher recognised that he had discovered a novel molecule.

Because he had isolated it from the cells nuclei, he named it nuclein, a name preserved in todays designation deoxyribonucleic acid.

Dahm says that in subsequent work Miescher showed that nuclein was a characteristic component of all nuclei and hypothesised that it would prove to be inextricably linked to the function of this organelle. He suggested that its abundance in tissues might be related to their physiological status with increases in nuclear substances preceding cell division. Miescher even speculated that it might have a role in the transmission of hereditary traits, but subsequently rejected the idea.

Dahm believes Mieschers discovery was a matter of serendipity and the prepared mind.

He had set out to characterise proteins and discovered DNA, which he recognised as being very worthy of further investigation. However, the breakthrough in thought that his discovery deserved only occurred half a century after his death, when the data necessary to fully grasp the significance of DNAs function were emerging. In many ways, Mieschers discovery was well ahead of its time.

Miescher died of tuberculosis on 26 August 1895.

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Friedrich Miescher gets ahead of the double helix - Cosmos

Throughout history 6 000 -- 7 000 plant species have been cultivated for food. Yet today 40 percent of our daily calories come from just three crops: rice, wheat and maize. Humans depend on little more than 30 plant species, many of which are struggling in the face of today's environmental changes. With biodiversity and entire ecosystems in serious decline, the International Treaty on Plant Genetic Resources for Food and Agriculture plays an increasingly important role in promoting farmers and their essential contribution to diversifying the crops that feed the world. The Treaty was negotiated by FAO and the Commission on Genetic Resources for Food and Agriculture (CGRFA) and adopted in 2001 to create a global system that provides farmers, plant breeders and scientists with access to plant genetic materials.

The genetic material in each variety of species is unique and precious. Derived from human and natural selection for many decades, these genetics are fundamental to our future of food. Genetic material ensures agricultural biodiversity and gives different species the ability to cope with changes, whether it be climate change, new pests and diseases, drought and even flooding. The Treaty's Benefit-sharing Fund invests in projects that conserve and develop crop genetic resources to improve food security in cooperation with farmers.

Here are three examples of how this Treaty has helped farming communities in developing countries cope with climate change and other environmental threats.

1. Exchanging and developing biodiverse potato varieties in Peru, Nepal and Bhutan

There are over 4 000 native varieties of potato growing in the Andean highlands. These varieties are well-adapted to harsh conditions and a changing climate. In contrast, Nepal and Bhutan have only two locally adapted potato varieties but face similar conditions and environmental threats as the Andes. With this in mind, the project sought to reduce the vulnerability of these mountain communities by introducing potatoes that are more resilient to extreme temperatures and offer better nutritional quality. Working closely with the International Potato Centre in Peru, farmers in Nepal and Bhutan became directly involved in selecting new, high-yielding, resilient and biodiverse varieties of potato. The genetic material from these potatoes has since been conserved, multiplied and used by national agricultural research systems in all three countries.

** 2. Conserving plant genetic resources to improve food and nutrition in Zimbabwe, Malawi and Zambia

Being heavily reliant on the success of the maize crop, communities in Zimbabwe, Malawi and Zambia have in recent years faced a severe food shortage because maize crops have been unable to withstand the effects of climate change, such as higher temperatures and torrential rains. "Because of the changing climate, our farm was producing less food, and most crops have not been doing so well apart from millet and sorghum," explained Lovemore Tachokere, a smallholder farmer from Malawi. Through the Benefit-sharing fund and the introduction of 159 Farmer Field Schools across the three countries, farmers were given support and a voice. They started introducinglost varieties of different crops, creating diversity in their fields that also ensured more varied and nutritious diets. As part of the project a total of 300 lost or forgotten small grain crop varieties were retrieved from national, regional and international gene banks as part of the Treaty's Multilateral System. These seeds are now available to farmers and scientists for further study and the development of new climate-smart varieties.

3. Ensuring a resilient cassava crop in Tanzania and Kenya

Cassava is the third largest source of carbohydrates in the world, playing a particularly important role in agriculture in sub-Saharan Africa because it does well in poor soils and with low rainfall. Additionally, because it is a perennial, cassava acts as a famine reserve. In recent years, however, extreme temperatures, drought, flooding and a new virus, provoking 'brown streak disease', have affected cassava cultivation in the region. In Tanzaniaand Kenya, a project implemented through the Benefit-sharing Fund has led to new, more resistant and tolerant cassava breeding lines, including 30 that are heat and disease tolerant. While the farmers are now experimenting with planting new cassava varieties and using improved agricultural practices, breeders and scientists have access to improved plant material from which to select essential genetic material for future use. Community seed banks have been established through the Benefit-sharing Fund in conjunction with Farmer Field Schools and are an important initiative to collect and conserve local crop varieties. They function as a platform for farmers to control and make informed decisions on the conservation of agrobiodiversity and the cultivation of a variety of crops with nutritional value.

In the 15 years since it came into force, the International Treaty hosted by FAO has created the largest global gene pool for sharing plant material for food and agriculture, the Multilateral System of Access and Benefit-sharing (MLS). The Benefit-sharing Fund has supported over one million people through 80 agricultural development projects in 67 developing countries. These projects are clear examples of how effective the sharing of skills and knowledge across continents can be and they are crucial in the race to meet the Sustainable Development Goals (SDGs), in particular SDG 15 (Life on Land) and SDG2 (Zero Hunger). Projects under the Benefit-sharing Fund are an indication that FAO's Strategy on mainstreaming biodiversity across agricultural sectors is already taking shape and showing positive results, demonstrating that the greater the diversification of crops, the more food secure a community can become and the more resilient they find themselves in the face of current threats like climate change, pests and disease.

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Enhancing food diversity in the midst of a climate crisis: How plant genetic material ensures future food security - Kenya - ReliefWeb

Data revealed 32 new sites on the human genome where variations in DNA appear to alter the risks of getting breast cancer, according to a study published inNature Genetics.

This analysis of genetic studies covering 266,000 women is the first to link these specific risk variants to multiple, detailed subtypes of breast cancer.

The findings from this analysis enhance our understanding of the biology that differentiates subtypes and may improve our ability to predict womens breast cancer risks, even at the level of specific breast cancer subtype, said corresponding author Nilanjan Chatterjee, PhD, in a press release.

Of the 32 new risk variants identified by researchers, 15 were also independently linked to 1 or more specific breast cancer subtypes. Of that specific set of 15 variants, 7 were linked to estrogen receptor status, 7 to tumor grade, 4 to HER2 receptor status, and 2 to progesterone receptor status.

Five of these newly identified subtype-specific risk variants are linked to greater risk for some breast cancer subtypes, but a lower risk in others.

The study incorporated data from over 100 breast cancer studies from the last 15 years found in the Breast Cancer Association Consortium. This analysis used new methods to identify DNA variants that have heterogeneous effects across subtypes. These DNA variants, such as Luminal-A and triple negative, can be defined by various tumor characteristics.

This data is paramount to the scientific understanding of the genetic architecture of breast cancer. Even more, this data will allow oncologists to calculate accurate risk scores for women based on their variant combinations.

Each one of these variants has a small apparent effect on breast cancer risk, and there may be a substantial effect when a person has a combination of them, Chatterjee said in a press release.

More than 250,000 women are diagnosed with breast cancer annually in the United States, with over 40,000 deaths. Before the analysis, researchers had identified over 170 gene variants that either increase or lower risk of breast cancer.

The hope for the further identification of gene variants is to inform women as much as possible in regard to their likelihood of developing breast cancer. And if their risk is high, it allows women to be screened more frequently.

Moving forward, the researchers hope this data can open avenues to exploring the underlying biological pathways that drive cancer. How each risk-linked DNA variation impacts gene activity and signaling networks in cells is crucial information to identifying risk levels for women.

These variants are special and if followed up properly may lead to important insights into the biology of these breast cancer subtypes, Chatterjee said in a press release.

Reference:

Genome Study Links DNA Changes to the Risks of Specific Breast Cancer Subtypes [news release]. Published May 18, 2020. https://www.jhsph.edu/news/news-releases/2020/genome-study-links-dna-cha.... Accessed May 20, 2020.

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Data Reveals DNA Variations that Alter Breast Cancer Risk in Women - Cancer Network

In 1994, researchers found two chimpanzees dead in Cte dIvoires Ta National Park, which holds West Africas largest rainforest. Autopsies of the chimpanzees revealed signs of hemorrhage resembling those found in humans during outbreaks of ebolavirus that occurred decades earlier in Zaire and Sudan. Indeed, further studies led to the designation of Ta Forest ebolavirus, one of five known strains of the virus that can lead to the ebolavirus disease. One researcher in the park contracted the disease during this time.

This is one of many stories of a zoonotic disease, also referred to as a zoonosis, which is a disease transmitted to humans by animals. Zoonoses are transmitted via direct or indirect contact with an infected individual, consuming contaminated food or water, or through vectors for example, being bitten by a mosquito carrying the disease.

The focus on transmission to humans dominates the global narrative of zoonoses, which include West Nile, rabies, Lyme and others. But certain pockets of the zoological research community focus on the reverse: humans transmitting zoonoses to wildlife, known as zooanthroponosis or anthroponosis.

In the current case of COVID-19, researchers of non-human primates have sounded alarm bells for the risks humans pose for transmitting SARS-CoV-2, the viral pathogen that causes the COVID-19 or coronavirus disease, to species of primates, including monkeys and apes. Being among some of the worlds most endangered species, of particular concern are wild great apes, including bonobos, eastern and western gorillas, orangutans and chimpanzees.

These types of outbreaks can have really devastating effects on primate populations, says says Amanda Melin, a biological anthropologist who runs the Primate Genomics and Ecology lab at the University of Calgary. This is a great example of the risks that we pose to other animals in the earth.

So far, there have been no positive tests of COVID-19 in wild great apes but the deadliness of the disease, should transmission occur, is likely high.

Its the quickest study Ive ever been involved in, says Melin of a study she co-led with Mareike Janiak, a postdoctoral scholar in molecular anthropology, and James Higham, a primate evolutionary biologist at New York University, that helps dispel the guesswork of which non-human primate species are at greatest risk. The study was conducted within about seven days in early April and posted to a preprint server shortly thereafter because of the urgency of its findings, which examine the genetics behind how the SARS-CoV-2 pathogen triggers the COVID-19 disease itself.

In order for a viral pathogen to take hold in a host, the proteins on its surface must bind with certain proteins on the surfaces of a hosts cells. Once the pathogens protein has found its cellular protein match, known as a receptor, the pathogen can enter the cell and trigger the disease. Coronavirus pathogens not just of COVID-19, but of other coronaviruses as well express spike proteins on their surfaces.

If the viruss protein cant find anywhere to bind, then its not going to become infectious, Melin puts simply.

Genes determine which proteins are formed on which cells. Melins study examines the coding sequence of the ACE2gene, which codes the cellular protein (the ACE2 receptor) for the SARS-CoV-2 pathogen. These receptors are found in endothelial tissues throughout the body, including in the lungs, hence the diseases respiratory effects.

As is the case concerning most forms of life, less diversity means less resilience to threat, and so too does it go for genetic predisposition to COVID-19.

Proteins are made of amino acids. Genes can vary in the sequences of their comprising DNA, and the variants of a gene will code protein receptors with different structures of their amino acids. Receptors with a range of structures make it more difficult for a pathogen to find its match.

With that context, consider this statement from Melins study: Here, we show that all apes, including chimpanzees, bonobos, gorillas, and orangutans, and all African and Asian monkeys, exhibit the same set of twelve key amino acid residues as human ACE2.

In other words, we and many of our primate cousins are in the same boat of being highly susceptible because we have highly similar ACE2 genes and receptors, making it easier for the SARS-CoV-2 pathogen to find its binding match on our cells.

Interestingly, the study found that monkeys in the Americas, and some tarsiers, lemurs and lorisoids, had more ACE2 genetic variation, indicating that many species are likely less susceptible. However, Melin warns, some lemur species are also likely to be highly susceptible, which is worrying as they are also among the most endangered primates.

(Bats, notorious for being hosts and spreaders of coronaviruses, have exceptionally high ACE2 genetic variation. Within just the handful of bat species that we looked at, we saw genetic variation equivalent to the variation we saw across the entire range of other mammals we included, says Melin.)

Its easy to imagine that were closely related to other non-human primates, and so we should be careful with diseases. But knowing that they have the exact same sites and should be equally susceptible to us, and seeing what its doing to humans around the world its really concerning.

At the end of 2016 and into early 2017, chimpanzees in the Ta forest were seen with cold-like symptoms. While it did not prove deadly, the illness was found by researchers to have been a coronavirus passed to the chimpanzees from humans, likely poachers.

Similar to Gombe, disease is the leading challenge for conservation of chimpanzees at Ta, says Thomas Gillespie, whose work with wild great apes in Africa includes directing theGombe Ecosystem Health Project, in addition to running the Gillespie Lab at Emory University. Because of that, were always alert to the risk of disease exposure from people. The Ta team, 10 years ago or so, had a major respiratory outbreak that killed all the young chimpanzees

The tell-tale signs of COVID-19 are likely also the same for human and non-human primates, namely dry cough and fever.

We expect to see human-like symptoms, or more extreme versions of those. Laboratory-based infection of macaques resulted in similar disease progression to what were seeing in humans, says Gillespie.

Because best practices of wildlife conservation, and especially with wild great apes, demand limited human interaction, researchers rely on technology to check animals for symptoms from a safe and hidden distance. Laser thermometers are used to check fecal masses immediately after defecation to determine body temperatures. Blood meals from mosquitos are tested to keep track of pathogens circulating between them and animals. Carrion flies, which feast on dead animals, can give insights on mortality.

The Cross River gorillas, for example we never see them because theyre very cryptic, says Gillespie of the critically endangered species. Only an estimated 200 or 300 remain, residing at the border of Nigeria and Cameroon. But the flies are still going to find them. Flies are going to let us know if theres a spike in mortality. And then that can alert us to potential issues.

Should COVID-19 begin to be found in wild great apes, there is good and bad news. The bad is that quarantining isnt an option. Because of group dynamics, individual animals within most groups cannot be removed They dont respond well it tends to go quite badly, says Gillespie making the likelihood of virus spreading to the entire group of a single infected animal quite high.

And, once a wild animal has left the wild, he adds, there are tremendous threats involved with putting them back in the wild because we might have exposed them to additional pathogens in the sanctuary setting.

So we cant think about things like darting individuals, removing them from the group, quarantining them. We have to really focus on them not becoming infected. And thats the most important thing.

Gillespie nonetheless expects the virus to make its way into at least some populations of wild apes populations. The key now is to understand how it is likely to spread among species, based on exposure as well as the apes behavior and ecology. For example, in some places, habituated apes those accustomed to proximity to humans might be exposed to SARS-CoV-2, but will likely never come into contact with non-habituated apes. In other areas, this might not be the case.

And in yet other areas, monkeys that share habitats with apes baboons and vervet monkeys in Africa; macaques in Asia might spread the virus among great ape groups, or act as intermediaries, carrying the virus from humans to great apes.

This is something were actively working on, says Gillespie, who is leading a team focused on creating a model of sites across Africa and Asia to guide location-based best practices for ape conservation during the pandemic. Were modeling the different ape species, including variables like demographics, behavioral ecology, and proximity to humans and other susceptible species. This can all influence the dynamics of transmission to wild great apes.

Many protected areas inhabited by wild great apes have quickly developed lockdown measures of their own, such as shutting down tourism, logging and mining operations and extensively testing staff and researchers.

One of the major efforts currently addressing this is led by the Primate Specialist Group and the Wildlife Health Specialist Group, both of the International Union for Conservation of Nature. The two groups released a joint statement in early March, listing ways that humans can minimize risks to wild great apes, including disinfecting their footwear, wearing surgical masks, quarantining when coming from abroad, and immediately leaving an area when feeling the need to cough or sneeze and not returning.

But for local communities who depend on the use of certain forests, current measures might mean theyre left without a livelihood. To this end, the IUCN has created a task force, which includes Gillespie, focused on COVID-19s impacts on areas where wildlife and communities share and depend on the same ecosystems. One component of this effort has been distributing funds to communities that might otherwise be forced to resort to actions that could threaten wildlife.

Melins and Gillespies studies and others like them are proving crucial tools for these conservationists to know where and how to allocate resources to protect species highly vulnerable to the disease, as well as provide scientific backing to policy- and decision-makers about the vulnerability of these species.

Even after the heightened phase of the pandemic has lessened, changes must continue to be made, she says: For primate observational research, we need to continue to be really careful about quarantining ourselves and about our proximities, always using best practices when were interacting with non-human primates. More generally, I hope we can slow and then stop the illegal trade of wildlife, which might help prevent future, different outbreaks.

And then she broadens her thoughts: How will it feel collectively, as humans, if were responsible for the rapid extermination of these species from the Earth?

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What the genetics of COVID-19 mean for the survival of wild great apes - Landscape News

The difference in COVID-19 death rates between white people and black, Asian and minority ethnic (BAME) people in the UK is shocking. One recent report found that, between the beginning of February and the end of April 2020, black people in England were 71% more likely than white people to die from COVID-19. And Asian people were 62% more likely.

This disparity has led to an inquiry by Public Health England and funding for urgent academic research into the issue. We expect many factors to be involved, including the disadvantages that BAME people face due to greater chances of poverty and health issues.

But its important that we examine whether there may also be a genetic component to the problem in order to fully understand whats going on. My colleagues and I are conducting research among frontline healthcare workers to try to see if there are any innate differences in the way different peoples immune systems respond to this specific virus, including genetic differences that may be associated with ethnicity.

Researchers have identified a greater chance of dying from COVID-19 among BAME people in several countries aside from the UK, including Norway and the US. There are many social reasons why ethnic minorities may generally be more vulnerable to disease, including a greater chance of malnutrition, more exposure to pollution due to where they live, or greater likelihood of working in less healthy environments.

Inequality and poverty also play a role in the fact that BAME people are more likely to suffer conditions that we know are linked to a greater chance of dying from COVID-19, such as diabetes and heart disease.

Initial data suggests that BAME healthcare workers are more likely to die from COVID-19 than their white colleagues. British Medical Association research has found that BAME doctors are twice as likely as white doctors to feel pressured into working with inadequate PPE when they are at risk of infection. And they are twice as likely not to feel confident enough to raise concerns about workplace safety.

However, all these established facts alone dont seem to explain why the risks of COVID-19 vary between different ethnic groups and are lowest among white people. This is particularly the case when we compare it with other forms of viral pneumonia that do not lead to such a difference.

The study that found BAME people in England were more likely to die from the disease accounted for differences in some underlying health conditions that are strongly linked to social issues, suggesting these werent the main factor. But the preliminary results from another study suggest ethnic minorities arent more likely to die once other factors linked to deprivation are taken into account.

To clarify this issue, its important to examine whether there may be some genetic component that predisposes ethnic minorities to a higher risk to COVID-19, while still recognising the critical role of other factors.

The way peoples immune systems work depends on genetic factors, not just environmental and social ones. There are effectively two parts to our immune systems. One is the part that produces antibodies, called the adaptive immune system. When our body has never seen a virus before, it can take several days for it to produce them, which is why some people get sick in the first place.

We also have an innate immune system that acts before our body has had time to make antibodies. This system is strong in children and young people, but not very good after the age of 65. This is likely to be one reason why older people are at higher risk of dying of COVID-19.

When a virus like the coronavirus SARS-CoV-2 enters a cell, molecules called toll-like receptors, or TLRs, alert the immune system that something potentially harmful is present. Interestingly, many of the bodys TLRs that can detect viruses come from genetic instructions found in the X chromosome, for which men have only one copy and women two.

We know that women can have a more effective innate immune response to other viruses such as HIV than men, and that oestrogen, the female hormone, enhances this type of immune response. We also know that women are less likely to die from COVID-19 than men.

Just as there are variations in DNA that are responsible for the differences in response of immune cells between the sexes, there can also be variations between people of different ethnic backgrounds. For example, the amount and type of genes that immune cells produce when the TLR-virus pathway is stimulated, are very different between people of African and of European origin.

This is not surprising, because we know that human populations from different parts of the planet have had to adapt to different types of infections. Ethnic differences in the risk to other respiratory viral diseases have been linked to genetic variation, and these variants are different in BAME groups and white people in these same pathways. However, the role of ethnicity in genetic susceptibility to viral diseases is still controversial.

We want to see if it could be a factor in the higher rate of BAME deaths from COVID-19. To do this, we are taking blood from frontline healthcare workers of a variety of ethnic backgrounds, assessing DNA differences and measuring the various substances the samples contain. The results could indicate if differences in the innate immune systems of BAME groups result in higher risk of developing severe COVID-19.

If there is some genetic element to the different death rates from COVID-19 between ethnic groups, its important that we understand it to give us the best chance of fighting the disease. For example, if we do find that the way the innate immune system works plays a role, we can advise people on ways to improve that system, such as through what we eat.

But that wont change the fact that the generally worse health among BAME groups in western societies is strongly linked to socioeconomic factors that are known to play a very significant role in this pandemic.

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Coronavirus: BAME deaths urgently need to be understood, including any potential genetic component - The Conversation UK