Friday, March 21, 2025

 

Revolutionizing cassava breeding: CRISPR-Cas9 unlocks potential for disease resistance and enhanced yield




Maximum Academic Press




By successfully applying CRISPR-Cas9 to enhance disease resistance, drought tolerance, and starch content, the study paves the way for more efficient cassava breeding programs.

Cassava (Manihot esculenta Crantz, 2n = 36) is one of the most important root crops globally, particularly in tropical regions of Africa, Asia, and Latin America. It is a major source of food, livestock feed, and industrial products. However, cassava cultivation faces numerous challenges, such as low yields, vulnerability to pests and diseases, and poor nutritional quality. While traditional breeding methods have been employed to address some of these issues, progress has been slow, and they often fail to produce significant improvements.

study (DOI: 10.48130/tp-0024-0046) published in Tropical Plants on 11 February 2025 by Qiuxiang Ma and Peng Zhang’s team, Chinese Academy of Sciences, represents a breakthrough in crop biotechnology and offers a promising pathway for future applications of genome editing in cassava and other important crops.

The research uses the CRISPR-Cas9 genome-editing tool to enhance cassava’s resistance to diseases, tolerance to drought, and starch content. The study identifies and targets critical genes associated with cassava mosaic disease (CMD), cassava brown streak disease (CBSD), drought stress response, and starch biosynthesis. By introducing precise edits into these genes, the researchers were able to develop cassava plants with enhanced resistance to both CMD and CBSD, which are two of the most destructive diseases affecting cassava crops globally. Additionally, edited cassava plants exhibited improved drought tolerance, an essential trait in light of the growing challenges posed by climate change. The study also reports that genome-edited cassava plants showed increased starch content, which is beneficial both for food security and industrial applications such as bioethanol production. The application of CRISPR-Cas9 technology in this context offers several advantages, including increased precision, faster breeding cycles, and the creation of genetically improved varieties without the introduction of foreign DNA, which may address concerns in regions with stringent regulatory policies.

In conclusion, the research highlights the potential of genome editing to transform cassava breeding and contribute to the improvement of this vital crop. These advancements could lead to increased cassava yields, improved nutritional quality, and greater resilience to climate change and disease. The findings of this research have significant implications for global food security, particularly in developing regions where cassava is a key staple.

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References

DOI

10.48130/tp-0024-0046

Original Source URL

https://doi.org/10.48130/tp-0024-0046

Funding information

This work was supported by the National Natural Science Foundation of China (32072118, 32160398), Central Public-interest Scientific Institution Basal Research Fund (NO. 1630052024001), and the Earmarked Fund for China Agriculture Research System (CARS-11).

About Tropical Plants

Tropical Plants (e-ISSN 2833-9851) is the official journal of Hainan University and published by Maximum Academic Press. Tropical Plants undergoes rigorous peer review and is published in open-access format to enable swift dissemination of research findings, facilitate exchange of academic knowledge and encourage academic discourse on innovative technologies and issues emerging in tropical plant research.

 

Pollutants often originate in the air





Paul Scherrer Institute

Imad El Haddad 

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Imad El Haddad is head of the Atmospheric Molecular Processes group in the Laboratory for Atmospheric Chemistry at PSI’s Center for Energy and Environmental Sciences. For his new study of the formation of organic aerosols, he led a team of more than 70 researchers from Europe and North America. © Paul Scherrer Insitut/Mahir Dzambegovic

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Credit: © Paul Scherrer Insitut/Mahir Dzambegovic





At CERN, the European Organisation for Nuclear Research in Geneva, an international research team led by the Paul Scherrer Institute PSI has conducted especially precise measurements of atmospheric chemistry. Through this study the researchers were able to show how harmful particulate matter arises from vehicular emissions and biomass combustion. Their findings are helping to make existing models of particle formation more accurate.

 

Anthropogenic organic aerosols are carbon-containing particles emitted by humans into the air, which are classified as particulate matter. They pose a significant health threat and contribute to millions of deaths worldwide each year. Especially in large cities, incomplete combustion processes from transportation, industry, and households produce exhaust gases that form harmful, respirable particles.

In an international study at CERN, the European Organisation for Nuclear Research in Geneva, researchers led by PSI have gained new insights into the formation of these organic aerosols. Their results show that such pollutants often form only after several oxidation steps. This suggests that pollution with anthropogenic particulate matter has a greater regional impact than previously assumed. This in turn suggests that it is not enough to simply reduce direct emissions from factories, homes, and vehicles, for example, with particulate matter filters. Rather, the precursor gases from which harmful organic aerosols later form must also be controlled. The researchers report their findings in the journal Nature Geoscience.

Human-made particulate matter forms more slowly

Researchers previously assumed that organic aerosols form through a single oxidation step. Natural precursor gases such as terpenes and isoprene – hydrocarbons emitted by plants – quickly add oxygen and thus directly form solid airborne particles.

However, the new study reveals that anthropogenic emissions behave differently. The precursor gases—such as toluene and benzene from automobile exhaust and organic material combustion—undergo multiple oxidation steps before forming solid particles. «This finding challenges the previous assumption that pollutants form primarily near the emission sources,» says Imad El Haddad, project leader of the new study. «It shows instead that anthropogenic aerosols undergo a longer formation process whereby their impacts extend regionally.»

A unique simulation chamber

The new study was conducted at CERN's CLOUD (Cosmics Leaving Outdoor Droplets) simulation chamber. More than 70 researchers from Europe and North America collaborated to simulate urban air pollution and track the formation of organic aerosols. The CLOUD facility is the cleanest atmospheric simulation chamber in the world and enables researchers to control parameters such as temperature and pressure with extreme precision – the temperature to approximately one-tenth of a degree. Its stainless steel cylinder has a capacity of approximately 26 cubic metres. High-precision sensors ensure that changes inside the cylinder can be observed down to the second. For their experiments, the researchers filled the chamber with a gas mixture resembling urban smog to trace the transformation of exhaust gases into organic aerosols.

Working in shifts, the researchers continuously measured the simulated urban smog. They determined the size distribution of the forming particles using a technique known as mobility analysis and determined the molecular identity of the condensing vapours in real time using mass spectrometry. They also precisely tracked what proportions of precursor gases and their products condensed on the chamber walls. This must be taken into account in calculations for pollutant formation. «Thanks to the precise observations, we are now better able to understand how anthropogenic aerosols form and grow in the air,» says El Haddad.

More precise predictions

The bottom line of the study is that a significant proportion of anthropogenic organic aerosols forms not after the initial oxidation, but only after additional oxidation steps that can take between six hours and two days. The research team estimates that this multi-step oxidation accounts for more than 70 percent of the total anthropogenic organic aerosol pollution.

Their results can improve air pollution models by enabling more accurate predictions of particulate matter concentrations, providing a better understanding of regional impacts. They also underscore the importance of controlling not only the direct emission of particulate matter, for example, through particle filters, but also the emission of precursor gases that later form solid particles. This could help to combat air pollution more effectively and thus improve public health.

Text: Jan Berndorff

 

 

Contact

Dr. Imad El Haddad
Center for Energy and Environmental Sciences
Paul Scherrer Institute PSI

+41 56 310 29 95
imad.el-haddad@psi.ch
[English]

 

Microplastic pollution disrupts photosynthesis, threatening global food security




Chinese Academy of Sciences Headquarters
Global maps of annual production losses for three main food crops 

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Global maps of annual production losses for three main food crops

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Credit: DANG Fei




A research group led by Prof. DANG Fei from the Institute of Soil Science of the Chinese Academy of Sciences, in collaboration with Prof. ZHONG Huan from Nanjing University, has uncovered a significant yet often overlooked consequence of microplastic pollution: its detrimental impact on photosynthesis—a critical process underpinning Earth's primary productivity and food security.

The study, recently published in PNAS, provides a comprehensive evaluation of the relationship between microplastic exposure and photosynthesis across terrestrial, marine, and freshwater ecosystems.

Microplastics—defined as plastic debris smaller than 5 mm—contaminate environments from deep-sea sediments to mountain glaciers. Despite growing awareness of this environmental hazard, the effects of microplastics on photosynthesis at the ecosystem level have remained unclear.

Previous studies have produced fragmented or contradictory results due to ecosystem complexities, differences among affected photoautotrophs (e.g., plants and algae), and the diverse nature of microplastics themselves. This knowledge gap poses a significant challenge to global efforts to achieve the United Nations (UN) Sustainable Development Goals (SDGs), particularly the Goals of Zero Hunger (#2), Good Health and Well-being (#3), Responsible Consumption and Production (#12), and Life Below Water (#14).

By analyzing 3,286 records using meta-analysis and machine learning techniques, the researchers quantified the global decline in photosynthesis due to microplastic exposure. Their findings reveal that microplastics decrease photosynthetic efficiency by 7.05–12.12% across terrestrial plants, marine algae, and freshwater algae. These reductions translate to estimated annual global losses of 4.11–13.52% (109.73–360.87 MT·yr-1) for key staple crops such as rice, wheat, and maize.

In aquatic ecosystems, microplastic-induced photosynthesis inhibition is projected to cause net primary productivity (NPP) losses of 0.31–7.24% (147.52–3,415.11 MT C·yr-1), leading to seafood production declines of 1.05–24.33 MT·yr-1. These figures underscore the hidden yet profound threat that microplastic pollution poses to global food security.

Encouragingly, the study suggests a pathway for mitigation. The researchers estimate that a 13% decrease in environmental microplastic levels could reduce photosynthesis losses by approximately 30%, preventing global losses of 22.15–115.73 MT·yr-1 in major crops and 0.32–7.39 MT·yr-1 in seafood production.

The findings highlight the urgent need to address microplastic pollution as a critical factor affecting global primary productivity. The study emphasizes the importance of incorporating plastic pollution mitigation strategies into broader sustainability and food security initiatives. It also calls for greater data collection and publication on the extent and mechanisms of microplastic-induced photosynthesis disruptions in future field studies.

As more high-quality field data and advancements in remote sensing technologies become available, researchers can refine their understanding of this emerging threat. These insights can then inform international plastic treaty negotiations and support efforts to achieve the UN SDGs.

A conceptual framework that allows the continual updating of data input to ameliorate our model’s precision and accuracy

Credit

DANG Fei

 

People from disadvantaged backgrounds have COVID-19 symptoms for longer




King's College London





People from disadvantaged backgrounds are more likely to experience COVID-19 symptoms for longer, new research suggests.

The research from King’s College London by authors funded by the National Institute for Health and Care Research (NIHR) reveals that social factors such as education level, financial stability, and the areas where people live played a significant role in whether individuals reported recovery from the virus more than a year after infection.

The research analysed data from over 3,800 participants across two UK cohorts: the COVID Symptom Study Biobank and TwinsUK. Using a questionnaire, participants were asked if they still had symptoms after having COVID-19.

Analyses revealed that participants with fewer social and economic advantages at the start of the pandemic were more likely to have ongoing symptoms. Women with lower education levels living in the most deprived areas had the lowest predicted probability of recovery, while men with higher education levels in less deprived areas were the most likely to feel fully recovered. Recovery rates varied between 73% and 90% in TwinsUK, and between 55% and 80% in the COVID Symptom Study Biobank, which had a larger proportion of people with long COVID.

The findings were published today in BMJ Public Health.

The inequalities in recovery were not explained by pre-existing health conditions but instead linked to broader social disadvantages. Financial and employment instability during the pandemic further contributed to poorer outcomes, suggesting that the impact of COVID-19 extended beyond physical health to economic and social wellbeing.

Dr Nathan Cheetham, Senior Postdoctoral Data Scientist at King’s College London and lead author of the paper, explains: “Inequalities in health between people who are more or less advantaged within society aren’t new, but this study is the first to look at the association between multiple socio-demographic factors and recovery from COVID-19.

“It’s very likely that social factors also influence the ability to recover from other illnesses and manage other long-term conditions, which makes addressing social disadvantage even more crucial.” 

This research adds to growing evidence that health outcomes are shaped by social factors, reinforcing the need for policies that address healthcare access and economic inequality. The findings come at a time when many people are still living with the long-term effects of COVID-19, highlighting the importance of continued support for those struggling to recover.

Professor Claire Steves, Professor of Ageing and Health at King’s College London and senior author on the paper, said: “This research emphasises how social factors affect long-term health outcomes. Disadvantaged groups don’t just experience more severe illness - they also face additional challenges when it comes to recovery.” 

Dr Cheetham and the team are building on these findings by investigating how different social backgrounds influenced people’s experiences of healthcare during the pandemic. Early results suggest that those in more deprived areas had greater difficulty accessing care, particularly for long COVID, with access to GP appointments being the most common barrier. With this additional work, the team hopes to provide further insight into how inequalities in healthcare access may have affected long-term recovery from COVID-19.

The research received funding from several sources including the NIHR-UKRI funded Convalescence study into long COVID.

Read the full study: https://bmjpublichealth.bmj.com/content/3/1/e001166

 

Deadly bacteria developed the ability to produce antimicrobials and wiped-out competitors




University of Pittsburgh
Emma Mills 

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Emma Mills, a microbiology and immunology graduate student at the University of Pittsburgh School of Medicine

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Credit: Emma Mills




A drug-resistant type of bacteria that has adapted to health care settings evolved in the past several years to weaponize an antimicrobial genetic tool, eliminating its cousins and replacing them as the dominate strain. University of Pittsburgh School of Medicine scientists made the discovery when combing through local hospital data – and then confirmed that it was a global phenomenon.

The finding, published today in Nature Microbiology, may be the impetus for new approaches in developing therapeutics against some of the world’s deadliest bacteria. It also validates a new use for a system developed at Pitt and UPMC that couples genomic sequencing with computer algorithms to rapidly detect infectious disease outbreaks.

“Our lab has a front row seat to the parade of pathogens that move through the hospital setting,” said senior author Daria Van Tyne, Ph.D., associate professor of medicine in Pitt’s Division of Infectious Diseases. “And when we took a step back and zoomed out, it quickly became apparent that big changes were afoot with one of the world’s more difficult-to-treat bacteria.”

The Enhanced Detection System for Healthcare-Associated Transmission (EDS-HAT) analyzes the genetic signatures of infections in hospitalized patients and flags patterns, allowing clinicians to intervene and stop potential outbreaks in real-time. But lead author Emma Mills, a microbiology and immunology graduate student in Van Tyne’s lab, realized that EDS-HAT was also a treasure trove of detailed historic information that she could mine to learn about the evolution of bacteria over time.

Mills focused on vancomycin-resistant Enterococcus faecium (VREfm), so-called because it can’t be eradicated with the popular antibiotic vancomycin. VREfm kills about 40% of the people it infects and is a particular plague on immunocompromised and hospitalized patients, who are often taking antibiotics that decrease the diversity of bacteria in their microbiomes, allowing drug-resistant bacteria, such as VREfm, to thrive.

After analyzing the genomic sequences of 710 VREfm infection samples from hospitalized patients entered into EDS-HAT over a six-year time span, Mills discovered that the variety of VREfm strains had shrunk from about eight fairly evenly distributed types in 2017 to two dominant strains that began to emerge in 2018 and, by the end of 2022, were the culprit in four out of every five patient VREfm samples.

Upon closer examination, Mills found that the dominant strains had acquired the ability to produce a bacteriocin, which is an antimicrobial that bacteria use to kill or inhibit one another. They’d weaponized this new capability to destroy the other VREfm strains, giving them unfettered access to nutrients for easier reproduction.

This further sparked Mills’s curiosity: If this was happening at the local hospital, was it happening elsewhere? No prior research publications had explored the possibility that this was a global phenomenon, so she consulted a publicly available library of more than 15,000 VREfm genomes collected globally from 2002 through 2022. Sure enough, what she’d observed locally had also been happening on a global scale.

“This was a completely unexpected discovery – I was surprised to see such a dramatic signal,” said Mills. “Once these strains are in an institutional setting – such as a hospital – and are matched up against other strains of VRE in a patient’s gut, they take over. It’s a ‘kill your buddies and eat their food’ scenario.”

Van Tyne said the finding doesn’t have immediate clinical consequences – it does not appear that the bacteriocin-wielding VREfm are making patients any sicker than their predecessors did. But it could point to potential avenues for the development of new therapies.

“The diversity of the VRE population appears to be narrowing from lots of different types causing infection to only a few. That means we may soon have only one single target for which to design therapeutics such as antibiotics or phage therapy,” Van Tyne said. “It also suggests that bacteriocins are very potent and perhaps we could weaponize them for our own purposes.”

Additional authors of the study are Katharine Hewlett, Alexander B. Smith, Ph.D., and Joseph P. Zackular, Ph.D., of Children’s Hospital of Philadelphia; and Marissa P. Griffith, Lora Pless, Ph.D., Alexander J. Sundermann, Dr.P.H., and Lee H. Harrison, M.D., of Pitt.

This research was funded by National Institutes of Health grants R01AI165519, R01AI127472 and R35GM138369.