Saturday, October 17, 2026

Chromosome-level genomes of two Magnoliales species provide new insights into the holocentric transition

Institute of Botany, Chinese Academy of Sciences

Chromosome-level genome assemblies and comparative multi-omics analyses of Cananga odorata and Myristica fragrans. — image:
Comparative genomics of holocentric *Myristica fragrans* and monocentric *Cananga odorata* reveals contrasting centromere, repeat, epigenetic, and genome-evolution landscapes.
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Credit: Jinyin Xing and Xing Guo

Beijing—Most plants pack their centromere into a single region of each chromosome, but a few Magnoliales species instead spread centromeric function along the entire chromosome. To understand the genomic basis of this difference, a research team from Northeast Forestry University and BGI Research assembled chromosome-level genomes for the holocentric species Myristica fragrans (nutmeg) and the monocentric species Cananga odorata (ylang-ylang), and compared them using integrated multi-omics analyses. The study was published in Journal of Systematics and Evolution.

“Most plants concentrate their centromere in one region of each chromosome, but some Magnoliales species have spread centromeric function along the whole chromosome,” says Jinyin Xing, first author of the study. “By comparing a holocentric species with a closely related monocentric one at the chromosome level, we could dissect the genomic changes underlying this remarkable reorganization.”

Two chromosome-level genomes, two ways to build a centromere

The team generated a 637 Mb, 22-chromosome assembly for M. fragrans and a 717 Mb, 8-chromosome assembly for C. odorata, both with high completeness (BUSCO 97.5%–98.6%). Hi-C contact maps confirmed the expected distinction: each C. odorata chromosome showed a single prominent heterochromatic block, a classic monocentric centromere feature, whereas M. fragrans showed no such concentrated signal, consistent with holocentric chromosomes. In silico centromere prediction with two independent tools recapitulated this pattern, identifying one centromere locus per chromosome in C. odorata but multiple loci per chromosome in M. fragrans.

Despite these structural differences, centromere-associated regions in both species were positively correlated with mCG/mCHG methylation and heterochromatin-related (B) chromatin compartments. The two species differed markedly elsewhere: C. odorata showed clustered heterochromatin and a dominant TE-rich plateau of LTR/Gypsy elements (Tekay, Athila, and SIRE), whereas M. fragrans displayed a dispersed chromatin organization with multiple discrete peaks of LTR/Copia elements (Ale and SIRE). Notably, mCHH was depleted within M. fragrans centromeres but enriched around those of C. odorata.

Shared centromere features, divergent repeat and methylation landscapes

The two major tandem-repeat families of M. fragrans (MF_351 and MF_269) were preferentially localized to chromosome termini, where they showed elevated mCG and mCHG, suggesting a structural role in chromosome stability. By contrast, tandem repeats in C. odorata accumulated predominantly in euchromatic regions, with negligible occupancy in heterochromatin.

Phylogenomic and Ks analyses showed that M. fragrans and C. odorata share an ancient whole-genome duplication (LAURb, ~115 million years ago), and that M. fragrans and M. yunnanensis also experienced two distinct waves of transposon expansion. These results suggest that the emergence of holocentricity is unlikely to be explained by a whole-genome duplication event alone.

The core kinetochore protein CENH3 is highly conserved between the two species, with only subtle lineage-specific differences in the centromere-recognition loop1 and N-terminal tail. The elongated NASP N-terminus appears to be a Magnoliales-wide feature rather than a holocentric signature, and no large-scale structural changes were detected in other core kinetochore proteins.

Lineage-specific rewiring, not a simple whole-genome story

Taken together, these results suggest that lineage-specific remodeling of repetitive sequences and epigenetic states, rather than whole-genome duplication or major changes in core kinetochore proteins, likely drove the reorganization of centromeric architecture in Myristica. The chromosome-level genomes and comparative framework generated here offer a foundation for future studies of chromosome biology and centromere diversification in non-model plant lineages.

Original Source:

Jinyin Xing, Qiongqiong Lin, Dongming Fang, Lingling Lin, Fang Wang, Jingwei Zhou, Handong Su, Wen-Bin Yu, Gang Hao, Tong Wei, Xing Guo. 2026. Comparative genomics with de novo genome assembly of two Magnoliales species: Insights into monocentric-to-holocentric transition. Journal of Systematics and Evolution 64(5): 929-947.

https://doi.org/10.1111/jse.70124

Keywords:

centromere evolution, comparative genomics, holocentromere, Magnoliales, transposable elements.

Author’s Institution:

Northeast Forestry University is a national key university in China recognized for its research strengths in forestry, life sciences, and ecology. BGI Research is a leading genomics research institute under BGI Group, specializing in genomics, multi-omics, and bioinformatics.

About JSE:

Journal of Systematics and Evolution (JSE) is a peer-reviewed, bi-monthly international English-language journal dedicated to the understanding of biodiversity and evolution. Papers in any of the following and related fields will be considered: systematics and biodiversity conservation, paleobiology and biogeography, adaptation, speciation and domestication, evolutionary genomics and Evo-Devo, theory and methods in evolutionary biology.

Journal

Journal of Systematics and Evolution

DOI

10.1111/jse.70124

Article Title

Comparative genomics with de novo genome assembly of two Magnoliales species: Insights into monocentric-to-holocentric transition

Researchers develop new AI tool to better predict stroke risk

New AI model analyses DNA to identify genetic risk factors for stroke, paving the way for more personalised prevention and treatment.

University of Technology Sydney

Researchers from the University of Technology Sydney (UTS) have developed an AI model that analyses a person’s DNA to better identify genetic risk factors for stroke, paving the way for more personalised risk assessments.

Stroke is the second leading cause of death worldwide. Around 46,000 Australians have a stroke each year, with one in three survivors experiencing moderate to severe disability, including long-term impairment.

First author, Dr Yue (Eric) Yang, who recently completed a PhD in Artificial Intelligence at UTS, said the AI tool is unique because it not only identifies genetic variants linked with stroke, but also considers their location in the genome and how they might interact.

“A stroke happens when blood flow to the brain is cut off or severely reduced, usually by a blood clot, which causes brain cells to die. Genetic susceptibility plays an important role in stroke risk, along with lifestyle factors such as smoking and alcohol consumption.

“We tested our AI model using genetic and health data from the UK Biobank, and also against health records from a large US-based database (All-of-us). Our model was more accurate than previous genetic risk tools at distinguishing people who had suffered a stroke from those who had not.”

The recently published study, Predicting risk of ischaemic stroke: A transformer model using genomic data, identified 18 genetic variants associated with ischaemic stroke, the most common type of stroke.

The researchers found that people with the highest genetic risk score had a 22% higher chance of stroke, compared to the lower risk group.

The study pointed to the gene EDEM2 in brain cortex tissue as a key contributor to stroke susceptibility, which could provide a specific target for further biological research into the causes of stroke.

The team used a type of AI known as a transformer, which is the technology behind large language models such as ChatGPT, to train the model on thousands of genetic variations and identify links to ischaemic stroke.

Distinguished Professor Jie Lu, Director of the Australian Artificial Intelligence Institute and Australian Laureate Fellow in the UTS Faculty of Engineering and IT, said the research highlights how AI can be used to develop personalised healthcare.

“AI can be used to find associations between human genes and disease, and build personalised risk assessments, to help prevent a potentially life-changing or fatal event,” said Professor Lu, who is also the Australian Industry Laureate Fellow in AI-for-Women’s Health.

“Genetics are only one part of stroke risk. The ability to combine a genetic score with clinical and lifestyle information, including established risk factors such as blood pressure, age, atrial fibrillation, type 2 diabetes and cholesterol, could enhance monitoring and prevention.

“We are now working on a multimodal AI tool that can combine a genetic risk assessment with other modes of data including health and lifestyle surveys, scans and imaging, to better assess risk in stroke and other diseases such as endometriosis.”

Corresponding author, Dr Kairui Guo has been working with the stroke unit at Liverpool Hospital in Sydney on genomic data analysis, as well as AI applications for acute stroke management, with support from neurologist and co-author Associate Professor and Senior Staff Specialist Dennis Cordato, who has provided clinical insights.

“When someone has a stroke, particularly at a young age, they often want to know whether other family members are also at risk. These new AI tools will provide the ability to better help families understand that risk,” said Dr Guo.

“We currently have a proposal for a preventative clinical trial. The aim is to recruit the first cohort of patients, sequence their genome, and analyse stroke risk. We are also interested sex differences in stroke risk between men and women.

“Traditionally, in thinking about stroke risk, genetics hasn’t been a main consideration, however this study highlights the significant impact of genetic factors. Without AI, it would be impossible to process that much data at an individual level to provide a personalised assessment.”

Journal

Computer Methods and Programs in Biomedicine

DOI

10.1016/j.cmpb.2026.109625

Method of Research

Computational simulation/modeling

Article Title

Predicting risk of ischemic stroke: A transformer model using genomic data

Article Publication Date

17-Sep-2026

COI Statement

The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: Jie Lu reports financial support was provided by Australian Research Council. If there are other authors, they declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

The pain-sensing receptor behind chili-pepper burn may hold clues to pain treatments

New study finds the body's capsaicin receptor, TRPV1, responds differently to varying triggers

University of California - Davis Health

Jie Zheng UC Davis School of Medicine — image:
By showing how capsaicin receptors respond to triggers, Jie Zheng hopes to open the door to new pain medicines.
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Credit: UC Regents

Scientists have long known that capsaicin, the ingredient that makes chili peppers feel hot and is used in some pain-relief creams, works by activating a pain-sensing receptor known as TRPV1.

New research from the UC Davis School of Medicine reveals that the receptor does not respond to every trigger in the same way. Instead, different stimuli appear to place TRPV1 into distinct functional states. The finding opens new possibilities for more targeted pain treatments.

The study, published in PNAS (Proceedings of the National Academy of Sciences), was led by researchers in the UC Davis Department of Physiology and Membrane Biology. The findings challenge a longstanding assumption that TRPV1 adopts a single activated state regardless of what triggers it.

TRPV1 as a potential target for pain medicine

TRPV1 is often called the body's capsaicin receptor. Located on pain-sensing nerve cells, it detects heat, tissue injury, inflammation and chemical compounds — including the capsaicin in hot peppers.

Because TRPV1 plays a central role in pain pathways and does not involve opioid signaling, it has long been considered a potential target for developing nonaddictive pain medicines. However, efforts to block the receptor have been complicated by its equally important role in regulating body temperature.

"Researchers have generally assumed that once TRPV1 is activated, the channel enters essentially the same open state regardless of what stimulus triggered it," said first author Bo Hyun Lee, a former researcher in the Zheng Lab at UC Davis. "Our findings show that the receptor is more sophisticated than that. Different stimuli appear to stabilize different open states, each with distinct functional properties."

Methods measured receptor’s response to different stimuli

To investigate how TRPV1 responds to different stimuli, the researchers measured electrical currents passing through individual channels activated by:

Capsaicin, the compound that gives chili peppers their heat
Resiniferatoxin, an extremely hot compound derived from a succulent plant
Hydrogen ions (protons), which create acidic conditions commonly associated with tissue injury and inflammation
2-APB, a chemical commonly used to modify ion channel activity
Heat

They found that different activators consistently produced different conductance levels. This finding suggests the channel opens in distinct ways rather than entering a common activated state.

Modeling of the different states of the TRPV1 pore, including closed (left), capsaicin-activated (middle) and 2-APB-activated (right).

The team then combined several approaches to see if those different conductance levels reflected structural differences in the receptor itself.

Using sensitive ion-permeation measurements (which measure how quickly charged particles move across a barrier), the researchers detected evidence that different activators altered the shape of the channel pore. They also used a fluorescence-based technique in living cells that allowed them to watch different parts of the channel protein shift position as it responded to different stimuli.

Finally, computational modeling helped visualize how the receptor's structure changed when activated by different stimuli.

Together, these approaches pointed to the existence of multiple distinct open configurations of TRPV1.

"We were able to see consistent evidence from several independent experimental methods that the pore of the channel does not look exactly the same when activated by different stimuli," said senior author Jie Zheng, professor in the Department of Physiology and Membrane Biology. "That convergence of evidence gave us confidence that these are genuine functional states rather than experimental artifacts."

The researchers also made another unexpected discovery. When two stimuli were applied together, the channel opened more slowly instead of more quickly. The finding suggests that different activation mechanisms may sometimes interfere with one another, revealing an additional layer of complexity in how pain signals are processed.

By showing how capsaicin receptors respond to triggers, Jie Zheng hopes to open the door to new pain medicines.

Findings may have implications for pain and basic research

Previous attempts to target TRPV1 with drugs for pain relief have often caused unwanted side effects, including major disruptions in body temperature regulation. The new study suggests it may someday be possible to selectively target receptor states associated with painful stimuli while preserving those involved in normal heat sensation.

"Our study provides a conceptual framework for thinking about TRPV1 in a much more nuanced way," said Vladimir Yarov-Yarovoy, co-author and professor in the Department of Physiology and Membrane Biology. "If different forms of activation produce different functional states, we may eventually be able to design therapies that selectively affect pain-related activity while leaving other essential functions intact."

The study also offers insight into how proteins function when encountering nontypical stimuli.

The work provides a new understanding of one of the body's most important pain sensors. It offers a potential roadmap for developing safer, more precise analgesic therapies. More research is needed to translate the study’s findings into new treatments.

Additional authors include Shisheng Li, Simon Vu, and Zhihao Yao from UC Davis and Yuhua Tian from UC Davis and Qingdao University.

Resources

Journal

Proceedings of the National Academy of Sciences

DOI

10.1073/pnas.2614335123

Method of Research

Experimental study

Subject of Research

Cells

Article Title

Distinct functional open states of the polymodal nociceptor TRPV1

Article Publication Date

15-Oct-2026

Modeling of the different states of the TRPV1 pore, including closed (left), capsaicin-activated (middle) and 2-APB-activated (right).

Credit

UC Regents.

A smarter way to deploy healthcare workers during disease outbreaks

KeAi Communications Co., Ltd.

HOW DYNAMIC SCHEDULING REALLOCATES HEALTHCARE STAFF UNDER UNCERTAINTY — image:
How dynamic scheduling reallocates healthcare staff under uncertainty
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Credit: Wang Z., Tang S., Zhang J.

During disease outbreaks, healthcare systems often face rapidly changing medical demand and uneven distribution of healthcare workers across regions. While cross-regional support can help relieve local shortages, traditional deployment strategies may become less effective as disease conditions evolve. Furthermore, healthcare workers themselves may face infection risks, which can reduce the available workforce and further complicate resource allocation decisions.

In a recent study published in the Journal of Management Science and Engineering, a team of researchers from Shandong University and University of Science and Technology of China developed a dynamic scheduling approach to improve the deployment of healthcare workers during disease outbreaks. The study addresses an important question: how can healthcare resources be allocated efficiently when both medical demand and workforce availability are uncertain? The team’s findings offer new insights for healthcare managers and policymakers seeking to strengthen resource coordination during complex health crises.

The researchers first developed a multi-objective optimization model that considers healthcare worker infection risks and uncertain medical demand. “By incorporating disease development predictions and changes in available healthcare capacity, our model enables decision-makers to adjust deployment strategies as conditions change,” shares co-corresponding author Jianghua Zhang. “It also considers multiple management goals, including improving deployment efficiency, maintaining regional fairness, and satisfying healthcare needs.”

The researchers found that dynamic cross-regional scheduling can effectively reduce mismatches between healthcare worker supply and demand. “Compared with approaches that ignore workforce risks, our proposed method provides solutions that better reflect actual healthcare capacity during outbreaks,” says Zhang. “The model also remains more reliable when future medical demand is uncertain, helping decision-makers balance efficiency, fairness, and service needs.”

Notably, effective healthcare worker allocation requires strategies that can adapt to changing conditions rather than relying on fixed deployment plans. “Our study provides a quantitative approach to support more flexible and reliable healthcare resource management during public health emergencies,” adds Zhang.

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Contact author details: Jianghua Zhang, School of Management, Shandong University; School of Public Policy & Management, University of Science and Technology of China, zhangjianghua@sdu.edu.cn

The publisher KeAi was established by Elsevier and China Science Publishing & Media Ltd to unfold quality research globally. In 2013, our focus shifted to open access publishing. We now proudly publish more than 300 world-class, open access, English language journals, spanning all scientific disciplines. Many of these are titles we publish in partnership with prestigious societies and academic institutions, such as the National Natural Science Foundation of China (NSFC).

Journal

Journal of Management Science and Engineering

DOI

10.1016/j.jmse.2026.08.001

Method of Research

Computational simulation/modeling

Subject of Research

Not applicable

Article Title

Dynamic cross-regional scheduling of healthcare staff during infectious disease outbreaks: A multi-objective robust optimization model

COI Statement

The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

Natural plant compound rutin protects brain coordination related neurons from acrylamide caused damage

KeAi Communications Co., Ltd.

image:
Rutin attenuates acrylamide-induced cerebellar neurotoxicity and motor deficits via activation of the PI3K/AKT signaling pathway
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Credit: Yunjue Wang, Zhongyu Wang, Shuping Liu, Suqiu Dong, Junhua Yang, Lixia Li, Yuxin Ma, Jing Liu; Guangdong Pharmaceutical University.

Acrylamide forms when high‑heat cooking processes starchy foods such as potatoes and bread. Human exposure also occurs via industrial workplaces and tobacco. Notably, this chemical can damage the cerebellum, the brain region controlling balance and movement coordination, leading to unsteady gait, limb weakness and poor balance in exposed people.

In a study published in the Journal of Holistic Integrative Pharmacy, researchers from Guangdong Pharmaceutical University tested whether rutin — a widely‑existing natural flavonoid found in many plants — could defend cerebellar neurons against acrylamide harm using rat experiments.

Thirty‑six male rats were divided into four groups: control, acrylamide‑intoxicated model, rutin treatment, and rutin plus PI3K‑pathway‑inhibitor LY294002 group. Over three weeks, the team tracked animal movement behaviour, examined brain tissue structure and measured key protein and oxidative‑stress markers.

“Acrylamide poisons special Purkinje neurons inside the cerebellar cortex,” says senior and co-corresponding author Prof. Jing Liu from Guangdong Pharmaceutical University. “These vital cells keep our balance and coordinated movement working normally.”

In particular, the team's behavioural tests show rutin greatly improved walking, balance‑beam and rotating‑rod performance in acrylamide‑damaged rats. Rutin also preserved Purkinje neuron structure, boosted antioxidant capacity and turned on the protective PI3K/AKT molecular pathway.”

Yet when LY294002 was added to block PI3K/AKT activity, nearly all of rutin's neuroprotective benefits disappeared. “This tells us rutin's brain‑shielding effect largely depends on activating PI3K/AKT signalling and easing oxidative stress,” explains co‑corresponding author Dr. Yuxin Ma. “Our animal findings provide new mechanistic evidence for rutin as a candidate protective agent against acrylamide‑related nervous‑system harm, though further research is needed before clinical translation.”

###

Contact the author:

Jing Liu, Department of Human Anatomy, Histology and Embryology, School of Basic Medical Sciences, Guangdong Pharmaceutical University, Guangzhou, China; liulq1227@163.com.

Journal

Journal of Holistic Integrative Pharmacy

DOI

10.1016/j.jhip.2026.09.003

Method of Research

Experimental study

Subject of Research

Animals

Article Title

Protective effect of rutin on cerebellar cortical neurons in acrylamide intoxicated rats and its underlying mechanism.

COI Statement

The authors declare that they have no known competing financial interests or personal relationships that might have appeared to influence the work reported in this paper.