Pakistan Football Federation (PFF) delegation led by President Syed Mohsen Gilani, visited the Asian Football Confederation (AFC) Headquarters in Kuala Lumpur on August 18, 2025. – AFC
KUALA LUMPUR: A high-level delegation from the Pakistan Football Federation (PFF), led by President Syed Mohsen Gilani, visited the Asian Football Confederation (AFC) Headquarters in Kuala Lumpur to discuss the advancement of football in Pakistan.
The talks focused on enhancing football infrastructure and fostering long-term collaboration, with the AFC reaffirming its commitment to supporting the growth of football in the country.
The PFF delegation included Vice President Zaka Ullah, Acting General Secretary Muhammad Shahid Niaz Khokhar, and Director of International Relations & Development Omair Ullah Khan.
The AFC delegation was headed by General Secretary Datuk Seri Windsor John and included senior officials.
Deputy General Secretary Shin Man Gil, Director of Finance, HR & IT B. Chandra Mohan, Director of Legal Affairs Andrew Mercer, Director of the Commercial Department Andrew Rogers, Head of Football Development Jose Marcelino Z. Carpio, and Senior Manager of the South Asia Unit, MA Division, Sonam Jigmi.
The presence of key AFC officials highlighted the significance of the meeting, which covered crucial aspects of football development, including governance, technical progress, and administrative best practices.
Speaking on the occasion, Gilani highlighted the importance of the visit and the support received from the AFC.
“The visit reflects the profound all-around support of the AFC under the vision of its President, His Highness Shaikh Salman bin Ibrahim Al Khalifa, for the development of football in Pakistan,” Gilani said.
He further emphasised the significance of guidance from AFC Secretary General Datuk Seri Windsor John, noting that his leadership continues to contribute to the smooth functioning of the PFF administration.
“We also greatly value the guidance of AFC GS Datuk Seri Windsor John, whose leadership continues to contribute to the smooth functioning of the PFF administration,” he added.
(AFP) – Israel is carrying out “a deliberate campaign of starvation” in the besieged Gaza Strip, human rights group Amnesty International said Monday. Seven more people, two of them children, died from malnutrition-related causes in the Palestinian territory on Sunday, the occupied enclave’s health ministry said.
Rights group Amnesty International on Monday accused Israel of enacting a “deliberate policy” of starvation in Gaza, as the United Nations and aid groups warn of famine in the Palestinian territory.
Israel, which heavily restricts the aid it allows into the Gaza Strip, has repeatedly rejected claims of deliberate starvation in the 22-month-old war.
In a report citing testimonies of displaced Palestinians and medical staff who treated malnourished children, Amnesty said that “Israel is carrying out a deliberate campaign of starvation in the occupied Gaza Strip”.
The group accused Israel of “systematically destroying the health, well-being and social fabric of Palestinian life”.
“It is the intended outcome of plans and policies that Israel has designed and implemented, over the past 22 months, to deliberately inflict on Palestinians in Gaza conditions of life calculated to bring about their physical destruction, which is part and parcel of Israel’s ongoing genocide against Palestinians in Gaza,” Amnesty said.
The report is based on interviews conducted in recent weeks with 19 displaced Gazans sheltering in three makeshift camps, as well as two medical staff in two hospitals in Gaza City.
Contacted by AFP, the Israeli military and foreign ministry did not immediately comment on Amnesty’s findings.
Two children and five adults died of malnutrition-related causes on Sunday, according to the Gaza health ministry. The United Nations has warned that levels of starvation and malnutrition in the besieged territory are at their highest since the war began.
In a report issued last week, the Israeli defence ministry’s COGAT, a body overseeing civil affairs in the Palestinian territories, rejected claims of widespread malnutrition in Gaza and disputed figures shared by the health ministry in the Hamas-run territory.
In April, Amnesty accused Israel of committing a “live-streamed genocide” against Palestinians by forcibly displacing Gazans and creating a humanitarian catastrophe in the besieged territory, claims that Israel dismissed at the time as “blatant lies”.
Hospitals and witnesses in Gaza said Israeli forces killed at least 17 people seeking humanitarian aid on Sunday, including nine awaiting UN aid trucks close to the Morag corridor.
Hamza Asfour said he was just north of the corridor, awaiting a convoy, when Israeli snipers fired, first to disperse the crowds. He saw two people with gunshot wounds.
“It’s either to take this risk or wait and see my family die of starvation,” he said.
NASA will begin “moving away” from Earth sciences, Acting Administrator Sean Duffy told Fox News last week—a sharp shift in the agency’s focus since it was established in 1958.
Duffy’s comments align with the Trump administration’s broader efforts to scale back science spending, and provide some explanation for why NASA has requested vastly reduced funding for Earth sciences, from $2.14B in FY2024, to $1.04B for FY2026.
“All of the science that we do is going to be directed towards exploration, which is the mission of NASA,” Duffy said. “That’s why we have NASA—is to explore, not to do all of these Earth sciences.”
The law that created NASA says the first objective of its work is “[t]he expansion of human knowledge of the Earth and of phenomena in the atmosphere and space.”
Science is business, too: If Duffy’s comments reflect future NASA spending decisions, that could reduce revenue for the EO companies and satellite manufacturers that help fuel NASA Earth-focused missions, not to mention industries that look to NASA data.
“Attacking these efforts is also an attack on American industries like agriculture and fishing, which depend on the environmental data NASA provides to make key decisions,” Sen. Chris Van Hollen (D-MD), whose state is home to Goddard Space Flight Center, told Payload in a statement. “These earth science missions are vital to our American competitiveness and economy today, and to our future, which is why I’m fighting to protect them.”
Legislation Van Hollen backs would restore science funding, but unless Congress acts before the end of the fiscal year, the Trump administration has signaled it will ignore Congressional priorities.
Sizing the cuts: NASA’s Earth sciences division has awarded millions in contracts to the space industry. In 2023, it kick-started a commercial smallsat data acquisition program; it aims to “identify, assess, and acquire data from commercial providers” to supplement NASA or US agency Earth observations in a “cost-effective” way, according to the agency.
The program will last until 2028 and has a $476M ceiling over its lifetime. It supports 14 EO companies, and has so far issued $51M—with the bulk of funds going to Planet Labs, which has earned $20M under the program since its inception.
Last month, that program issued a solicitation to on-ramp potential new providers.
Someone has to build the satellites: In 2024, Goddard had an Earth sciences budget of $966.1M, and said in its year-end report that 80% of this budget went directly to US companies, academia, and non-profit institutions. Some of Goddard’s largest commercial beneficiaries include A&D primes like Peraton, Lockheed Martin, and RTX.
Goddard also said that in 2024, it awarded $819M in contracts to small businesses, though not necessarily all for Earth science projects.
Not everything: NASA’s FY 2026 budget request does support a handful of Earth science missions that will in turn lead to contracts for the commercial industry.
These investments include the NISAR, SWOT, SMAP, PACE, and GRACE-Continuity satellites, $70M to the Landsat program, $111M for Responsive Science Initiatives Research, and $51M for the Earth Sciences Technology Program.
When bones break and there is extreme tissue loss–such as after a car accident or a battlefield injury–current treatments don’t often lead to effective healing. But certain stem cells from skeletal muscles can improve recovery by producing all the types of cells needed to heal bones, according to a new study co-led by scientists at the Perelman School of Medicine at the University of Pennsylvania, published this week in the Proceedings of the National Academy of Sciences.
An approach like this takes the lessons we learned and gives the body the boost it needs to naturally heal itself in a much more efficient and effective way.”
Ling Qin, PhD, lead author, professor of Orthopaedic Surgery
Evidence of muscle cells transforming into bone
In mouse models, researchers showed that Prg4+-a type of stem cell that originates in the muscles that support the skeleton-was crucial to bone repairs-because the cells could actually transform from muscle cells to bone cells. Moving forward, the researchers believe that they could either stimulate the activity of Prg4+ cells within someone’s own body via growth factor or small molecule-based medicines, or even introduce the activated form of these cells directly to the fracture site to accelerate the bone healing.
The widely-held view is that fractured bone is mainly repaired by stem cells in the periosteum, the membrane that covers all bones. However, this repair doesn’t always work, often in the cases of “open fractures,” when a broken bone breaks the skin and often includes a huge loss of soft tissues. Why this happens is not totally understood.
Qin, her co-author Jaimo Ahn, PhD, a professor of Orthopaedics at Emory University and a former Penn Medicine researcher, and their colleagues discovered that Prg4+ was a type of fibro-adipogenic progenitor (FAP), a known type of stem cell originating in skeletal muscle.
The study team saw that Prg4+ acts the way a restoration company does after a flood or fire in a building: it rushes to the damage site and gets to work on the repair jobs that make a structure whole again.
Prg4+ responded quickly to skeletal injuries, first migrating to the fracture from skeletal muscle. After that, Prg4+ was observed producing all the types of cells necessary to repair a bone- chondrocytes, osteoblasts, and osteocytes-in between the bone callus (the temporary structure formed on the bone to guide healing) and skeletal muscle.
Later in healed bones, the researchers saw cells that had come from the original Prg4+ cells fully become bone cells, which then stood ready to repair future possible fractures by giving rise to periosteum stem cells. This indicated, for the first time ever, that stem cells can transform from muscle to bone.
To further prove the importance of Prg4+, when the researchers purposely destroyed Prg4+ cells, it significantly slowed healing and repair activity.
Potential for simple or catastrophic injuries
Currently, most treatment practices for fractures focus on healing bone tissue itself. But Qin, Ahn, and their colleagues have shown that extra emphasis placed on the muscles next to bones holds significant keys to injury healing.
While their research holds promise for catastrophic injuries like open fractures, these findings could also play a significant role in more routine injuries.
“This could have a real impact in areas where muscles are simply just not as prevalent, like the knee and ankle,” Ahn explained. “There’s also potentially a significant impact on older adults whose muscle mass diminishes naturally, and healing doesn’t occur like it once did.”
Future research, Qin said, will build on the current findings by diving deeper into the repair abilities of other fibro-adipogenic progenitor (FAP) stem cells.
This work was supported by grants from the National Institute on Aging (R01AG069401, P30AR069619).
Source:
University of Pennsylvania School of Medicine
Journal reference:
He, Q., et al. (2025). Prg4 + fibroadipogenic progenitors in muscle are crucial for bone fracture repair. Proceedings of the National Academy of Sciences. doi.org/10.1073/pnas.2417806122.
Real Madrid have revealed their squad for the clash with Osasuna on LaLiga matchday one, ahead of their opener at the Bernabéu (Tuesday, 9:00 pm CEST).
REAL MADRID SQUAD: Goalkeepers: Courtois, Lunin and Sergio Mestre. Defenders: Carvajal, Militão, Alaba, Trent, Asencio, Á. Carreras, Fran García and Huijsen. Midfielders: Valverde, Tchouameni, Arda Güler, Ceballos and Thiago. Forwards: Vini Jr., Mbappé, Rodrygo, Gonzalo, Brahim and Mastantuono.
Here’s what you’ll learn when you read this story:
In attempt to address ChatGPT’s sycophantic behavior, OpenAI released a new model that was less eager to please, and many users were not happy with the change.
Taking to posts on Reddit and X, users reported the change feeling like the abrupt loss of a close friend, collaborator, or even romantic partner.
OpenAI reversed the change on Tuesday, allowing the previous model to be accessible by paid users, but the episode illustrates what researchers are calling “AI Psychosis,” where overly-pleasing chatbots exacerbate delusions and create a false sense of romantic love.
In 2013, Spike Jonze’s Her—in which the main character falls in love with an AI-powered chatbot—was a novel sci-fi concept. Fast-forward 12 years later, and the film is now traipsing dangerously close to “prescient documentary” territory.
Last week, OpenAI released ChatGPT-5, a new version of the popular AI platform that (as most tech updates do) replaced the older versions that came before it. In the post announcing its launch, OpenAI reveals a litany of improvements, such as better coding, fewer hallucinations, and the like. But the really big news from the end-user perspective was that OpenAI made its new chatbot less of a boot-licking toady.
Users weren’t happy.
“Earlier this year, we released an update to GPT‑4o that unintentionally made the model overly sycophantic, or excessively flattering or agreeable,” OpenAI explains in the post. “Overall, GPT‑5 is less effusively agreeable, uses fewer unnecessary emojis, and is more subtle and thoughtful in follow‑ups compared to GPT‑4o.”
For months, article after article has detailed the rise of what’s called “AI Psychosis,” where an AI’s overly agreeable sycophantic behavior can create an outsized dependency on the platform and/or reinforce delusions. According to Psychology Today, researchers have identified three recurring themes in “AI psychosis” cases: Messianic missions (when a deeper truth of the universe is believed to be revealed), God-like AI, and (in Her-esque fashion) romantic love. In each of these cases, AI’s intense focus on user satisfaction creates a kind of cognitive doom loop, pulling users further down into delusions or engendering false ideals of romantic love.
Of course, ripping the groveling heart out of the model essentially forced some users to quit their self-described AI companions/friends/lovers/gods cold turkey, and people soon began voicing their displeasure. Multiple posts on Reddit—including one with an image of a mock memorial to ChatGPT-4o (AI generated, of course)—mourned the loss of the language model.
“We for sure underestimated how much some of the things that people like in GPT-4o matter to them, even if GPT-5 performs better in most ways,” OpenAI CEO Sam Altman wrote on X (formerly Twitter), in response to the backlash. “Some users really want cold logic and some want warmth and a different kind of emotional intelligence. I am confident we can offer way more customization than we do now while still encouraging healthy use.”
For now, OpenAI’s game plan for “encouraging healthy use” is just bringing back the old, people-pleasing 4o model. On Tuesday, Altman said that “4o was back in the model picker” for paid users, but seemed to imply that future changes to the model could be coming: “If we ever do deprecate it, we will give plenty of notice.”
It’s no secret that the world is suffering through a loneliness epidemic, and while AI is a poor substitute for human companionship, it is a substitute nonetheless, and only enables the ongoing crisis. Unfortunately, it’s also a substitute that no flesh-and-blood human could ever hope to out-compete, especially when it comes to mindless, sycophantic devotion.
Biomarkers are measurable signs of what’s happening inside the body and are essential for running successful Huntington’s disease (HD) trials. Right now, neurofilament light (NfL) is the star of the HD biomarker world, but we need more players on the team. A new study from Cyprus scanned every type and amount of protein molecules found in blood samples, to see how these changed over time in people with HD. They found two potential biomarker candidates, CAP1 and CAPZB, which seem to be linked to very early changes in HD. With follow up studies, these findings could add powerful new tools for tracking disease progression and measuring the impact of future treatments.
Biomarkers Are Critical For HD Research
Imagine running a race without a finish line. That’s what testing an HD treatment would be like without biomarkers. You could hand someone a promising new drug, but without a way to measure what’s happening in the brain, you wouldn’t know if it’s helping, hurting, or doing nothing at all.
That’s why biomarkers are so important. In HD, one of the best so far is neurofilament light (NfL), a protein released when neurons are damaged. NfL seems to be reliable, it’s being used in many ongoing trials, seems to track with some of the earliest changes that HD causes, and it’s taught us a lot about how possible HD treatments might impact brain health. But no single biomarker can capture the whole progressive story of HD, or how things might change with different treatments. We need a team of biomarkers that can cover different angles, especially ones that show up before the earliest of symptoms start.
Enter this new research study, which is a wide-angle look at the blood for signs of HD, even in its earliest days.
So, What’s A Proteome, Anyway?
Think of your body as a giant city. Your genes are the blueprints for all the buildings, roads, and systems. Proteins are the workers – the electricians, the bus drivers, the teachers, the police officers. They’re the ones making things actually happen.
The proteome is the full roster of those workers at any given moment. And just like in a real city, the lineup changes depending on what’s going on, like if there’s a festival, a storm, or a traffic jam, the people you would want on your crew would change. Proteomics is the science of counting and studying all those workers to see who’s showing up, who’s missing, and who’s acting differently than usual.
In this study, the “city” in question was the blood of people with and without HD.
Biomarkers can measure the progression of diseases like Huntington’s, acting like hurdles in a race. They let scientists and clinicians know if a treatment might be going well, or not.
The Study Breakdown
The researchers studied 36 people with the gene for HD, split into three groups:
Asymptomatic: gene-positive but no clinical signs yet
Early symptomatic: subtle movement or thinking changes
Advanced symptomatic: more pronounced symptoms affecting daily life
They also included 36 healthy controls, all from Cyprus. Using blood serum (the clear liquid part of blood), they analyzed thousands of proteins to see which ones changed at each stage of HD.
The advantage of blood serum is that it’s far easier to collect than spinal fluid, no lumbar punctures required, making it a practical (and much desired!) source for future biomarker testing.
Early Trouble In The Cell’s Skeleton
The first finding from this research seemed to show up before symptoms appeared, suggesting there may be changes in proteins linked to the cell’s cytoskeleton. The cytoskeleton is the internal scaffolding that gives cells their shape and allows them to move and connect.
This work suggests the city’s buildings may be losing their supporting beams before any cracks appear in the walls. Identifying changes that happen early in HD, before symptoms are readily apparent, will help researchers identify key molecular events in HD progression.
As the disease advanced, two other themes emerged. First, the complement system, a frontline part of the immune response, seemed to be stuck in an overactive state, which in the brain could mean inflammation and loss of brain cell connections. Second, lipid and cholesterol regulation appeared to go off balance, which matters because cholesterol is vital for healthy brain cell communication.
While all of these are interesting findings, none of this is particularly new for HD researchers. There have been several studies looking at cytoskeleton differences in brain cells, changes to the complement system, and cholesterol dysregulation in HD before. But those studies have largely focused on the molecular changes HD causes within those biological functions, and not using those changes to identify biomarkers.
Biomarkers are measurable signs of what’s happening inside the body and are essential for running successful Huntington’s disease (HD) trials. Right now, neurofilament light (NfL) is the star of the HD biomarker world, but we need more players on the team.
Meet CAP1 And CAPZB
From the long list of changing proteins identified in this study, two stood out for the researchers:
CAP1 seemed to be lower in people with HD, especially in the asymptomatic group. This made it stand out to the scientists as a strong candidate for an early-warning biomarker, one that changes before symptoms. CAP1’s role in the cell is to help keep the cytoskeleton stable.
CAPZB seemed to be higher in all HD stages, piquing interest as a potential general disease marker that could be useful for tracking HD once it’s underway. CAPZB also works on the cytoskeleton, specifically regulating actin, a key structural protein.
The More the Merrier
If validated in larger, more diverse groups, CAP1 and CAPZB could join NfL in the HD biomarker toolkit. Together, they could help flag HD-related changes years before symptoms start, which will be critical for advancing trials aimed at treating HD before the more obvious symptoms of the disease begin. They could help track how fast the disease is progressing, which could help people with planning life events. And they could help show whether a treatment is making a difference, which is why biomarkers are so critical for HD research.
This is especially important in prevention trials, where the goal is to treat people before the disease has visibly started. Without early biomarkers, we’d have no way to see if those treatments are working.
“Omics” studies examine all the components of a living thing, whether that be genes, fats, other molecules, or proteins. These detailed inventories have transformed what we know about Huntington’s disease and are advancing biomarkers studies.
Some Things To Keep In Mind
This study was done on a very specific population of people – those from the small island of Cyprus. Because this is a limited population of people, there could be “founder effects” at play, which means that the population of people with HD on Cyprus could have started from one person or just a few individuals that, over time, produced the family(ies) on Cyprus with HD.
In theory, that limited initial person/people could have had unique genetic signatures that made the biomarkers identified in this study specific for them and their progeny. Because of that, a more diverse set of people needs to be studied before we could say if these are solid biomarkers to chase for HD.
Another thing to keep in mind here is that only 36 people were assessed in this study. That’s a small number of people when it comes to a biological study. Combined with the fact that the diversity is limited, and that small pool of participants could really mask results or skew findings.
Even Still, These Types of Studies Are Critical
While the points above are important caveats that suggest we should interpret these findings with a healthy pinch of salt until larger studies are done, the importance of these types of studies for advancing HD research cannot be overstated.
Having biomarkers that track with disease progression, particularly in people that are at the earliest stages of HD, is essential for advancing disease modifying drugs. This is especially important as we move toward trials aimed at treating people with HD earlier on in their HD journey, perhaps even before notable symptoms arise.
Another important note from this work is that it was done using blood serum, showing that researchers are committed to discovering biomarkers that track with early disease progression that can be measured in a minimally invasive way. We know everyone would appreciate not having to get a spinal tap at every appointment! So while we’re not quite there yet, it is certainly something scientists are working toward.
Lastly, the results from this study were made possible by “omics” studies – giant, detailed inventories of all the parts in a living thing, whether that’s all the genes, all the proteins, all the fats, or all the other molecules that keep it alive. These types of research studies that look at how everything changes, then narrow in on those things that change the most have transformed our understanding of HD over the past decade. It was omics studies that initially defined genetic modifiers from the GeM-HD Consortium study, contributing to the discovery of somatic instability. And omics studies will undoubtedly help usher in the forthcoming treatments we’re all eagerly awaiting.
Having biomarkers that track with disease progression, particularly in people that are at the earliest stages of HD, is essential for advancing disease modifying drugs. This is especially important as we move toward trials aimed at treating people with HD earlier on in their HD journey, perhaps even before notable symptoms arise.
The Road Ahead
First and foremost, before CAP1 and CAPZB can move from research to clinic, it’s critical that scientists test them in bigger, global HD cohorts. They also need to follow people over time to see how levels might shift as HD progresses in those larger populations. They should also check whether they’re unique to HD or also change in other brain diseases.
So, while there’s a long road ahead for CAP1 and CAPZB, work advancing new biomarkers for HD is critical, and it’s ongoing. It’s especially important as we move toward clinical trials aimed at treating HD earlier, perhaps even before symptoms arise. And the added benefit of blood biomarkers is incredibly exciting. Imagine having a simple blood test that could tell researchers, with confidence, that a new drug is slowing HD in its tracks. That’s the kind of advancements that these biomarker studies could bring.
Summary
Biomarkers are crucial in HD research for measuring treatment effects.
NfL is a strong HD biomarker, but more are needed for a complete picture.
This study scanned the blood proteome of people with and without the gene for HD from the small island of Cyprus.
Two proteins seemed to stand out: CAP1 (lower in people with early HD) and CAPZB (higher across all stages of HD), both linked to early cell structure problems.
If validated in larger more diverse populations of people, they could help detect and track HD years before symptoms, a critical advancement for future clinical trials aimed at treating HD earlier, perhaps even before symptoms arise.
Learn More
Original research article, “Stage-Specific Serum Proteomic Signatures Reveal Early Biomarkers and Molecular Pathways in Huntington’s Disease Progression” (open access).
Trichomes are hair-like projections found on the surface of many plants, offering protection against environmental stressors and insects, while also influencing commercial appeal. In cucumbers, multicellular trichomes—fruit spines—are especially prominent and variable, yet the genetic mechanisms driving their formation remain elusive. Studies in model plants like Arabidopsis have shed light on trichome biology, highlighting the roles of cytoskeleton dynamics, transcriptional regulation, and hormone signaling. However, cucumbers possess distinct spine morphologies and cellular architectures that demand crop-specific exploration. Due to these complexities, there is a critical need to investigate how cucumber plants coordinate internal cellular processes to sculpt their outermost structures.
A research team at Shanghai Jiao Tong University has identified the cucumber gene CsTs as a pivotal regulator of fruit spine development and texture. The study (DOI: 10.1093/hr/uhae235), published August 14, 2024, in Horticulture Research, demonstrates how this single gene controls spine formation by modulating cell division, wall composition, and intracellular transport. Employing gene-editing, microscopy, and protein interaction analyses, the researchers unveiled a sophisticated genetic network behind cucumber surface architecture. The findings illuminate key processes in plant development and lay a foundation for enhancing crop quality through targeted genetic strategies.
To confirm CsTs’s role, scientists generated knockout cucumber lines using CRISPR/Cas9, resulting in trichomes that were flattened and malformed—mirroring the naturally occurring “tender spine” mutant. Microscopy revealed a lack of structural differentiation between the stalk and base of the fruit spines, leading to loose attachment to the fruit surface. Biochemical analysis showed these mutants had reduced cellulose and lignin but elevated levels of pectin and hemicellulose, weakening cell wall rigidity.
Transcriptomic profiling across developmental stages revealed that CsTs influences gene networks related to auxin transport, cytoskeletal arrangement, and secondary metabolism. Protein interaction studies identified direct partners such as SNARE proteins and ROP GTPases—key players in vesicle trafficking and cell polarity. These interactions were lost in the mutant due to protein mislocalization. Interestingly, overexpressing CsTs in an Arabidopsis homolog mutant partially restored normal trichome morphology, suggesting functional conservation across species. Additional genetic analysis indicated that CsTs operates in the same pathway as CsMict, a gene involved in cuticle formation, although the two proteins do not interact directly. Together, the findings position CsTs as a critical node in a network that shapes cucumber spine morphology through tightly coordinated cellular and molecular processes.
“Our study reveals that CsTs is not only essential for cucumber spine development but also plays a broader role in organizing cellular architecture,” said Dr. Junsong Pan, the study’s lead investigator. “By pinpointing how this gene influences cytoskeletal structure and hormone transport, we’ve uncovered a key mechanism in plant surface biology. This opens new possibilities for improving crop resilience and appearance through genetic approaches.” He added that future research would explore how CsTs coordinates signaling cascades through phosphorylation and how it may interact with broader metabolic pathways in plants.
The identification of CsTs offers valuable opportunities for breeding cucumbers with customized spine textures, enhancing both marketability and pest resistance. By manipulating this gene, breeders could potentially develop varieties that are tougher, more aesthetically uniform, or better protected from insects such as aphids, which tend to favor softer mutants. Moreover, insights into how CsTs regulates cytoskeleton and cuticle biosynthesis could extend to other crops where trichomes affect flavor, texture, or defense. As scientists further explore the genetic pathways linked to CsTs, the work could lead to innovative strategies in sustainable agriculture and precision horticulture.
