Study creates bacteria that consume carbon dioxide for growth

Agencies
November 30, 2019

Washington D.C., Nov 30: Researchers have developed bacteria called Escherichia coli, which consume carbon-di-oxide for energy instead of organic compounds.

This creation in synthetic biology highlights the incredible plasticity of bacterial metabolism and could provide the framework for future carbon-neutral bioproduction. The work appeared in the journal -- Cell.

"Our main aim was to create a convenient scientific platform that could enhance CO2 fixation, which can help address challenges related to the sustainable production of food and fuels and global warming caused by CO2 emissions," said senior author Ron Milo, at systems biologist at the Weizmann Institute of Science.

"Converting the carbon source of E. coli, the workhorse of biotechnology, from organic carbon into CO2 is a major step towards establishing such a platform," added Milo.

A grand challenge in synthetic biology has been to generate synthetic autotrophy within a model heterotrophic organism.

Despite widespread interest in renewable energy storage and more sustainable food production, past efforts to engineer industrially relevant heterotrophic model organisms to use CO2 as the sole carbon source has failed.

Previous attempts to establish autocatalytic CO2 fixation cycles in model heterotrophs always required the addition of multi-carbon organic compounds to achieve stable growth.

"From a basic scientific perspective, we wanted to see if such a major transformation in the diet of bacteria -- from dependence on sugar to the synthesis of all their biomass from CO2 -- is possible," said first author Shmuel Gleizer (@GleizerShmuel), a Weizmann Institute of Science postdoctoral fellow.

"Beyond testing the feasibility of such a transformation in the lab, we wanted to know how extreme an adaptation is needed in terms of the changes to the bacterial DNA blueprint," added Gleizer.

The researchers used metabolic rewiring and lab evolution to convert E. coli into autotrophs. The engineered strain harvests energy from formate, which can be produced electrochemically from renewable sources.

Because formate is an organic one-carbon compound that does not serve as a carbon source for E. coli growth, it does not support heterotrophic pathways.

They inactivated central enzymes involved in heterotrophic growth, rendering the bacteria more dependent on autotrophic pathways for growth.

They also grew the cells in chemostats with a limited supply of the sugar xylose -- a source of organic carbon -- to inhibit heterotrophic pathways.

The initial supply of xylose for approximately 300 days was necessary to support enough cell proliferation to kick start evolution. The chemostat also contained plenty of formates and a 10% CO2 atmosphere.

By sequencing the genome and plasmids of the evolved autotrophic cells, the researchers discovered that as few as 11 mutations were acquired through the evolutionary process in the chemostat.
One set of mutations affected genes encoding enzymes linked to the carbon fixation cycle.

The authors said that one major study limitation is that the consumption of formate by bacteria releases more CO2 than is consumed through carbon fixation.

In addition, more research is needed before it's possible to discuss the scalability of the approach for industrial use.

In future work, the researchers will aim to supply energy through renewable electricity to address the problem of CO2 release, determine whether ambient atmospheric conditions could support autotrophy, and try to narrow down the most relevant mutations for autotrophic growth.

"This feat is a powerful proof of concept that opens up a new exciting prospect of using engineered bacteria to transform products we regard as waste into fuel, food or other compounds of interest," Milo said.

"It can also serve as a platform to better understand and improve the molecular machines that are the basis of food production for humanity and thus help in the future to increase yields in agriculture," added Milo.

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News Network
February 12,2020

Washington, Feb 12: People who are optimistic may contribute to the health of their partners, staving off the risk factors leading to Alzheimer's disease, dementia and cognitive decline as they grow old together, according to a study.

The research, published in the Journal of Personality, followed nearly 4,500 heterosexual couples from the US Health and Retirement Study for up to eight years.

The researchers found a potential link between being married to an optimistic person and preventing the onset of cognitive decline, due to a healthier environment at home.

"We spend a lot of time with our partners.They might encourage us to exercise, eat healthier or remind us to take our medicine," said William Chopik, an assistant professor at the Michigan State University in the US.

"When your partner is optimistic and healthy, it can translate to similar outcomes in your own life. You actually do experience a rosier future by living longer and staving off cognitive illnesses," Chopik said.

An optimistic partner may encourage eating healthy foods, or working out together to develop healthier lifestyles, the researchers said.

For example, if a person quits smoking or starts exercising, their partner is close to following suit, they said.

"We found that when you look at the risk factors for what predicts things like Alzheimer's disease or dementia, a lot of them are things like living a healthy lifestyle," Chopik said.

"Maintaining a healthy weight and physical activity are large predictors.There are some physiological markers as well. It looks like people who are married to optimists tend to score better on all of those metrics," he said.

The researchers said there is a sense where optimists lead by example, and their partners follow their lead.

They also suggest that when couples recall shared experiences together, richer details from the memories emerge.

Chopik noted while there is a heritable component to optimism, there is some evidence to suggest that it's a trainable quality.

"There are studies that show people have the power to change their personalities, as long as they engage in things that make them change," Chopik said.

"Part of it is wanting to change. There are also intervention programs that suggest you can build up optimism," he added.

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Agencies
May 19,2020

New York, May 19: Cigarette smoke spurs the lungs to make more of the receptor protein which the novel coronavirus uses to enter human cells, according to a study which suggests that quitting smoking might reduce the risk of a severe coronavirus infection.

The findings, published in the journal Developmental Cell, may explain why smokers appear to be particularly vulnerable to severe COVID-19 disease.

"Our results provide a clue as to why smokers who develop COVID-19 tend to have poor clinical outcomes," said study senior author Jason Sheltzer, a cancer geneticist at Cold Spring Harbor Laboratory in the US.

"We found that smoking caused a significant increase in the expression of ACE2, the protein that SARS-CoV-2 uses to enter human cells," Sheltzer said.

According to the scientists, quitting smoking might reduce the risk of a severe coronavirus infection.

They said most individuals infected with the virus suffer only mild illness, if they experience any at all.

However, some require intensive care when the sometimes-fatal virus attacks, the researchers said.

In particular, they said three groups have been significantly more likely than others to develop severe illness -- men, the elderly, and smokers.

Turning to previously published data for possible explanations for these disparities, the scientists assessed if vulnerable groups share some key features related to the human proteins that the coronavirus relies on for infection.

First, they said, they focused on comparing gene activity in the lungs across different ages, between the sexes, and between smokers and nonsmokers.

The scientists said both mice that had been exposed to smoke in a laboratory, and humans who were current smokers had significant upregulation of ACE2.

According to Sheltzer, smokers produced 30-55 per cent more ACE2 than their non-smoking counterparts.

While the researchers found no evidence that age or sex impacts ACE2 levels in the lungs, they said the influence of smoke exposure was surprisingly strong.

However, they said, the change seemed to be temporary.

According to the data, the level of the receptors ACE2 in the lungs of people who had quit smoking was similar to that of non-smokers.

The study noted that the most prolific producers of ACE2 in the airways are mucus-producing cells called goblet cells.

Smoking is known to increase the prevalence of such cells, the scientists said.

"Goblet cells produce mucous to protect the respiratory tract from inhaled irritants. Thus, the increased expression of ACE2 in smokers' lungs could be a byproduct of smoking-induced secretory cell hyperplasia," Sheltzer explained.

However, Sheltzer said other studies on the effects of cigarette smoke have shown mixed results.

"Cigarette smoke contains hundreds of different chemicals. It's possible that certain ingredients like nicotine have a different effect than whole smoke does," he said.

The researchers cautioned that the actual ACE2 protein may be regulated in ways not addressed in the current study.

"One could imagine that having more cells that express ACE2 could make it easier for SARS-CoV-2 to spread in someone's lungs, but there is still a lot more we need to explore," Sheltzer said.

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Agencies
February 6,2020

Researchers have found the rates of lung cancer are higher in young women than men.

The study, published in the journal Pediatrics, examined lung cancer rates in young adults in 40 countries across five continents and uncovered a trend of higher lung cancer rates in women compared with men in recent years.

The emerging trend was widespread, affecting countries across varied geographic locations and income levels.

The changes appeared to be driven by a rising rate of adenocarcinoma lung cancer among women, said the study researchers from University of Calgary in Canada.

Lung cancer rates have been higher among men than women because men started smoking in large numbers earlier and smoked at higher rates; however, recent studies have reported converging lung cancer incidence rates between sexes.

Among men, age specific lung cancer incidence rates generally decreased in all countries, while in women the rates varied across countries with the trends in most countries stable or declining, albeit at a slower pace compared to those in men.

For the findings, lung and bronchial cancer cases between 30-64 age group from 1993-2012 were extracted from cancer incidence in five continents.

The study found the higher emerging rates of lung cancer in young women compared to young men.

According to the researchers, future studies are needed to identify reasons for the elevated incidence of lung cancer among young women.

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