Blazes that have torched tens of thousands of hectares of forest in France, Spain and Portugal have made 2022 a record year for wildfire activity in southwestern Europe, the EU’s satellite monitoring service said Friday.
Amid a prolonged heatwave that saw temperature records tumble, the Copernicus Atmosphere Monitoring Service (CAMS) said that France had in the last three months reached the highest levels of carbon pollution from wildfires since records began in 2003.
It follows Spain registering its highest ever wildfire carbon emissions last month.
CAMS said the daily total fire radiative power—a measure of the blazes’ intensity—in France, Spain and Portugal in July and August was “significantly higher” than average.
The service warned that a large proportion of western Europe was now in “extreme fire danger” with some areas of “very extreme fire danger”.
“We have been monitoring an increase in the number and resulting emissions of wildfires as heatwave conditions have exacerbated fires in southwestern France and the Iberian Peninsula,” said Mark Parrington, CAMS senior scientist.
“The very extreme fire danger ratings that have been forecasted for large areas of southern Europe mean that the scale and intensity of any fires can be greatly increased, and this is what we have been observing in our emissions estimates and the impacts it has on local air quality.”
CAMS released satellite imagery showing a plume of smoke from the huge in southwestern France extending hundreds of kilometres over the Atlantic.
France has received help battling the latest blaze—which is 40-kilometres (25 miles) wide and which forced some 10,000 people to evacuate the region—in the form of 361 firefighters from European neighbours including Germany, Poland, Austria and Romania.
Globally, 2022 is currently the fourth highest year in terms of wildfire carbon, CAMS said.
Scientists say heatwaves such as the exceptional hot and dry spell over western Europe are made significantly more likely to occur due to manmade climate change.
Researchers at the Francis Crick Institute have shown that an antibiotic used to treat tuberculosis (TB) is affected by pH levels in the environment the bacteria has infected.
In 2020 alone, it is estimated that TB led to the deaths of around 1.3 million people. While it is curable, the treatment involves taking a course of various antibiotics over at least six months and the drugs can have severe side-effects.
On infection with TB, the bacteria enter into a type of immune cell, called macrophages. One of the defense mechanisms these cells use is creating an acidic environment to kill the infecting agent.
In their study, published in mBio on World TB Day (24 March), the researchers developed a fluorescence-based imaging technique to study the effects of this acidic environment on both the bacteria and antibiotics. Using this approach, they were able to monitor, in real-time, the effects of changes in pH levels.
By experimentally changing pH levels in infected cells, they found that TB is able to maintain and regulate its own pH independently of the pH of the macrophage, providing a defense against the immune system.
The researchers then tested whether four front-line TB antibiotic treatments are affected by different acidity levels. They found that one antibiotic often used as part of the TB treatment regime, pyrazinamide, is only effective within an acidic environment.
Pierre Santucci, co-corresponding author and postdoctoral training fellow in the Host-Pathogen Interactions in Tuberculosis Laboratory at the Crick, says: “Understanding that the effectiveness of antibiotics can be impacted by environmental pH levels is really valuable. It underlines the importance of testing new treatments or treatment combinations in conditions which closely mimic what happens inside cells.”
The researchers also found that pyrazinamide affects the ability of TB to regulate its own acidity levels. Pyrazinamide is an important part of the TB treatment strategy as it reduces the length of time drugs need to be taken for.
Max Gutierrez, senior author and group leader of the Host-Pathogen Interactions in Tuberculosis Laboratory at the Crick, says: “With rising levels of antibiotic resistance globally, finding new, more effective treatments is crucial. This has been challenging, in part because TB lives inside cells, so any treatment has to be able to enter into the cells and work effectively in this intracellular environment.
“By understanding more about how current antibiotics are impacted by conditions inside of cells, such as acidity, we hope it could help the search for new drugs or better drug combinations.”
The researchers will continue this work studying how the environment within TB and macrophages affects antibiotics. And the imaging approach developed to monitor pH levels could be adapted to study other bacteria and parasites.
Pierre Santucci et al, Visualizing Pyrazinamide Action by Live Single-Cell Imaging of Phagosome Acidification and Mycobacterium tuberculosis pH Homeostasis, mBio (2022). DOI: 10.1128/mbio.00117-22
Research by Kai Jiao, M.D., Ph.D., and colleagues at the University of Alabama at Birmingham and in Germany has yielded fundamental insights into the causes of severe birth defects known as CHARGE syndrome cases. These congenital birth defects include severe and life-threatening heart malformations.
The researchers successfully inactivated the gene for CHD7 in the neural crest cells of mouse embryos, and then rigorously probed how this change in developing cardiac neural crest cells caused severe defects in the outflow tract and great arteries, leading to perinatal lethality. The heart defects in the embryos, and other birth defects, resembled human CHARGE syndrome defects. Human mutations in CHD7 are known to cause about 70 percent of CHARGE syndrome cases.
The study in Proceedings of the National Academy of Sciences, led by Jiao, co-corresponding author Karim Bouazoune, Ph.D., Philipps Universität Marburg, Marburg, Germany, and first author Shun Yan, Ph.D., a researcher V in Jiao’s lab, also clarifies a longstanding controversy. Previous attempts by others to alter CHD7 function in neural crest cells had failed to cause heart defects in several mouse models. This study’s improvement was use of better molecular scissors to delete a portion of the CHD7 gene.
A surprising finding in the current research was discovery of a new epigenetic function for CHD7, in addition to its well-established ATP-dependent chromatin remodeling activity. Chromatin is a DNA-protein complex consisting of the mammalian genome tightly wound around histone proteins to create a string of nucleosomes, like pearls on a necklace. Chromatin remodeling factors like CHD7 use the energy of ATP to remodel the chromatin, making selected genes available for expression. The turning-on and turning-off of select sets of genes is fundamental to embryonic development, during the time that a single fertilized egg grows into a complex fetus with at least 200 different types of cells, all originating from the same DNA genome, but differentiated using different gene programs.
In addition to the chromatin remodeling activity, Jiao and colleagues discovered that CHD7 acts in an ATP-independent fashion to recruit histone-modifying enzymes to target promoter or enhancer loci on the genome.
“Our findings strongly suggest that CHD7 can also directly recruit an H3K4 methyltransferase writer to target elements,” said Jiao, a professor in the UAB Department of Genetics. “The dual activities of CHD7 may represent an efficient mechanism to coordinate nucleosome remodeling and H3K4 methylation at these target loci. The mutual interaction between the CHD7 nucleosome remodeler and histone methylation machinery could form a positive feedback loop to stabilize epigenetic states at target elements.”
In other key findings of the study—in addition to showing an essential cell-autonomous role for CHD7 to regulate cardiac neural crest cell development—the researchers showed that a single point mutation in the CHD7 gene was sufficient to cause severe developmental defects and embryonic lethality in mammals. The researchers also used transcriptomic analyses to show that CHD7 fine-tunes the expression of a gene network critical for cardiac neural crest cell development. They followed that with a protein-protein interaction screen and found that CHD7 directly interacted with multiple developmental disorder-mutated proteins. One of these was WDR5, a core component of H3K4 methyltransferase complexes. That interaction with WDR5 led to the discovery of CHD7’s ability to recruit histone-modifying enzymes to target promoter or enhancer loci on the genome.
The researchers say that the CHD7 protein interactome suggests CHD7 is likely implicated in an even wider range of physiological processes and human diseases than previously anticipated.
“Importantly,” Jiao said, “we now provide a molecular framework of direct candidate interactors to investigate known or new CHD7 functions, as well as the molecular etiology of CHD7-associated diseases or phenotypes.”
The discovery of two different functions for CHD7 also could have clinical relevance. “Our data imply that patients carrying a premature stop codon versus missense mutations will likely display different molecular alterations,” Jiao said. “These patients might therefore require personalized therapeutic interventions.”
Shun Yan et al, CHD7 regulates cardiovascular development through ATP-dependent and -independent activities, Proceedings of the National Academy of Sciences (2020). DOI: 10.1073/pnas.2005222117
New activity found for CHD7, a protein factor vital in embryonic development (2020, December 3)
retrieved 3 December 2020
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