Daily Archives: June 30, 2020

Published 30 June 2020

A radical new way of thinking about soil has finally solved the mystery of why adding organic material like manure improves flood and drought resilience, climate control and crop yields - universal ecosystem services that are widely recognised as worth billions to the global economy.

Founded on more than 50 years worth of data from a unique field experiment, researchers have demonstrated that common farming practices drain the soil of carbon, altering the structure of soils microscopic habitat and, remarkably, the genetics of microbes living within it.

The team of microbiologists and physicists, led by Rothamsted Research, considered almost 9,000 genes, and used X-ray imaging to look at soil pores smaller than the width of a human hair, and in concert with previous work, have started forming what they envisage will be a universal Theory of Soil (see Notes).

In healthy soils, relatively low nitrogen levels limit microbes ability to utilise carbon compounds, so they excrete them as polymers which act as a kind of glue - creating a porous, interconnected structure in the soil which allows water, air, and nutrients to circulate.

Writing in the journal Scientific Reports, the researchers reveal that the Victorian-era switch from manure to ammonia and phosphorous based fertilizers has caused microbes to metabolise more carbon, excrete less polymers and fundamentally alter the properties of farmland soils when compared to their original grassland state.

Lead researcher Professor Andrew Neal said: We noticed that as carbon is lost from soil, the pores within it become smaller and less connected.This results in fundamental changes in the flow of water, nutrients and oxygen through soil and forces several significant changes to microbial behaviour and metabolism. Low carbon, poorly connected soils are much less efficient at supporting growth and recycling nutrients.

A lack of oxygen in soil results in microbes having to turn to nitrogen and sulphur compounds for their energy-inefficient processes, he says, which result in increased emissions of the greenhouse gas nitrous oxide among other issues.

The closed soil structure also means microbes need to expend more energy on activities such as searching out and degrading less easily accessible organic matter for nutrients.

Conversely, in carbon-rich soil there is an extensive network of pores which allow for greater circulation of air, nutrients and retention of water.

Professor Neal added: Manure is high in carbon and nitrogen, whereas ammonia-based fertilisers are devoid of carbon. Decades of such inputs - and soil processes typically act over decades - have changed the way soil microbes get their energy and nutrients, and how they respire.

Whilst soil carbon was already known to drive climate and water cycles the world over, it took a chance discussion between experts working at very different scales to discover the reason why.

The idea to look at this link between the living and non-living components of soil came about through a discussion between an expert in microbial genetics Professor Andrew Neal, and Professor John Crawford now at the University of Glasgow - who studies the way complex systems behave.

Despite carbons critical role, the mechanisms underlying carbon dynamics and the link to soil water were poorly understood, said Professor Neal.Society struggles with the concept of what soil is and how it can be managed effectively because it is such a complex combination of biological, chemical and physical processes.

We took inspiration from a theory proposed by Richard Dawkins in the 1980s that many structures we encounter are in fact products of organisms genes Dawkins used the examples of bird nests and beaver dams.This view helped us understand soil as a product of microbial genes, incorporating organic materials from plants and other inputs to create all-important structure.

We have shown for the first time a dynamic interaction between soil structure and microbial activity - fuelled by carbon - which regulates water storage and gaseous flow rates in soil with real consequences for how microbes respire.

The group, which also involved scientists from the University of Nottingham, are the first to seriously study the details of this intimate two-way relationship between the microscopic life in soil and its structure at scales relevant to microbial processes.

The results also demonstrated why soils can sometimes show great resilience to human interventions.

Although years of intensive management practices have altered what compounds microbes predominantly live on and increased the frequency of genes that allow this lifestyle, very few genes are ever completely lost from the system. That crucially allows soils to respond to changes and these results can really help with any future remediation efforts, said Professor Neal.

Microbes are very good at acquiring genes from each other, which is why rather than look at different species we looked at the abundance of different genes and what functions they ultimately coded for.

The results also have implications for farmers, where the addition of nitrogen and phosphorous fertilizers - and not carbon - may in fact be leading to a degradation of the natural fertility and the efficiency with which nutrients are processed in their soils that will be detrimental to the long term productivity of their farm.

The negative impacts of increased leakiness of the soil system include nutrient loss to the atmosphere and rivers.

More here:
And finally... Where there's muck, there's brass - Scottish Construction Now

Researchers have discovered that Mediterranean populations may be more susceptible to an autoinflammatory disease because of evolutionary pressure to survive the bubonic plague. The study, carried out by scientists at the National Human Genome Research Institute (NHGRI), part of the National Institutes of Health, determined that specific genomic variants that cause a disease called familial Mediterranean fever (FMF) may also confer increased resilience to the plague.

The researchers suggest that because of this potential advantage, FMF-causing genomic variants have been positively selected for in Mediterranean populations over centuries. The findings were published in the journal Nature Immunology.

Over centuries, a biological arms race has been fought between humans and microbial pathogens. This evolutionary battle is between the human immune system and microorganisms trying to invade our bodies. Microbes affect the human genome in many ways. For example, they can influence some of the genomic variation that accumulates in human populations over time.

"In this era of a new pandemic, understanding the interplay between microbes and humans is ever critical," said Dr. Dan Kastner, NHGRI scientific director and a co-author on the paper. We can witness evolution playing out before our very eyes.

One such microbe is Yersinia pestis, the bacterial agent responsible for a series of well-documented bubonic plague(link is external) epidemics that led to over 50 million deaths.

FMF, like the plague, is an ancient disease. It is the most common periodic fever syndrome, and symptoms of FMF include recurrent fevers, arthritis, rashes and inflammation of the tissues that line the heart, lungs, and abdominal organs. FMF may also lead to renal failure and death without treatment. The disease appears across the Mediterranean region and mostly affects Turkish, Jewish, Armenian and Arab populations.

Genomic variants in the MEFV gene cause FMF. MEFV encodes a protein called pyrin. In healthy people, pyrin plays a role in the inflammatory response of the body. Pyrin is activated when there is an immune response (for example, in the event of an infection). Pyrin increases inflammation and the production of inflammation-related molecules.

In contrast, FMF patients produce abnormal pyrin because of genomic variants (mutations) in the MEFV gene. Mutated pyrin does not need an infection or other immune trigger to be activated; rather, it is able to directly predispose people to seemingly unprovoked episodes of fever and inflammation.

The MEFV mutations also have other usual properties. Researchers have discovered that people with only one copy of a MEFV genomic variant that causes FMF do not get the disease. Also, prior to effective treatment, those with two copies have high mortality rate by the age of 40, but usually live long enough to have children.

Despite the lower survival rate, almost 10% of Turks, Jews, Arabs and Armenians carry at least one copy of an FMF-causing genomic variant. If chance were the only factor, that percentage would be much lower.

The researchers proposed that this higher percentage was a consequence of positive natural selection, which is an evolutionary process that drives an increase in specific genomic variants and traits that are advantageous in some way.

"Just like sickle cell trait is positively selected for because it protects against malaria, we speculated that the mutant pyrin in FMF might be helping the Mediterranean population in some way," said Jae Jin Chae, Ph.D., senior author of the paper and a staff scientist in NHGRI's Metabolic, Cardiovascular and Inflammatory Disease Genomics Branch. "The mutant pyrin may be protecting them from some fatal infection."

The team turned to Yersinia pestis, the infamous bubonic plague-causing bacterium, as a possible candidate for driving the evolutionary selection for FMF mutations in the Mediterranean population.

It turns out Yersinia pestis contains a particular molecule that represses the function of pyrin in healthy individuals. In doing so, the pathogen suppresses the body's inflammatory response to the infection. This way, the body cannot fight back.

"Inflammation is a process in which white blood cells protect the body from infection. From the host's point of view, inflammation helps us survive. From the bacteria's point of view, inflammation is something to be evaded by any means available," said Daniel Shriner, Ph.D., staff scientist in the Center for Research on Genomics and Global Health at NHGRI.

Researchers were struck by the fact that Yersinia pestis affects the very protein that is mutated in FMF. They considered the possibility that FMF-causing genomic variants may protect individuals from the bubonic plague caused by Yersinia pestis.

The idea that evolution would push for one disease in a group to fight another may seem counterintuitive. But it comes down to what is the least bad option.

The average mortality rate of people with bubonic plague over centuries has been as high as 66%, while, even with a carrier frequency of 10%, less than 1% of the population has FMF. Theoretically, the evolutionary odds are in the latter's favor.

But first, the team had to verify if two of the genomic variants that cause FMF had indeed undergone positive selection in Mediterranean populations.

For this, they performed genetic analysis on a large cohort of 2,313 Turkish individuals. They also examined genomes from 352 ancient archaeological samples, including 261 from before the Christian era. The researchers tested for the presence of two FMF-causing genomic variants in both groups of samples. They also used population genetics principles and mathematical modeling to predict how the frequency of FMF-causing genomic variants changed over generations.

"We found that both FMF-causing genomic variants arose more than 2,000 years ago, before the Justinian Plague and the Black Death. Both variants were associated with evidence of positive selection," said Elaine Remmers, Ph.D., associate investigator in NHGRI's Metabolic, Cardiovascular and Inflammatory Disease Genomics Branch.

Researchers then studied how Yersinia pestis interacts with FMF-causing genomic variants. They took samples of particular white blood cells from FMF patients. In addition, they took samples from people who carry just one copy of the genomic variants (hence, do not get the disease).

The team found that Yersinia pestis does not reduce inflammation in white blood cells acquired from FMF patients and people with one copy of FMF-causing genomic variants. This finding is in stark contrast to the fact that Yersinia pestis reduces inflammation in cells without FMF-associated mutations.

The researchers thought that if Yersinia pestis does not reduce inflammation in people with FMF, then perhaps this could potentially increase patients' survival rate when infected by the pathogen.

To test this hypothesis, the researchers genetically engineered mice with FMF-causing genomic variants. They infected both healthy and genetically engineered mice with Yersinia pestis. Their results showed that infected mice with the FMF-causing genomic variant had significantly increased survival as compared to infected healthy mice.

These findings, in combination, indicate that over centuries, FMF-causing genomic variants positively selected in Turkish populations play a role in providing resistance to Yersinia pestis infection. Whether the same is true for other Mediterranean populations remains to be seen. The study offers a glimpse into the unexpected and long-lasting influence of microbes on human biology.

ReferencePark, Y.H., Remmers, E.F., Lee, W. et al. Ancient familial Mediterranean fever mutations in human pyrin and resistance to Yersinia pestis. Nat Immunol (2020). https://doi.org/10.1038/s41590-020-0705-6.

This article has been republished from the following materials. Note: material may have been edited for length and content. For further information, please contact the cited source.

Read the original post:
Cause of Common Autoinflammatory Disease May Have Protected Ancestors From Plague - Technology Networks