NYU Abu Dhabi Reveals Hidden Biological Switch Linked to Obesity in New Study

Researchers at New York University Abu Dhabi (NYUAD) have identified a crucial protein acting as a hidden biological switch in fat cells, potentially unlocking new avenues for combating obesity. Published in the prestigious journal Cell Death & Disease on February 26, 2026, the study reveals how nuclear myosin 1 (NM1)—a chromatin-associated actomyosin motor—regulates gene expression and metabolic processes essential for healthy adipose tissue development.7271 This discovery highlights NYU Abu Dhabi's pivotal role in addressing the UAE's pressing public health challenges, where obesity rates are among the highest globally.

Obesity, defined as excessive fat accumulation that increases health risks (often measured by body mass index, BMI, above 30 kg/m²), affects over 30% of UAE adults, with projections indicating nearly 95% of those aged 25+ could be overweight or obese by 2050.9384 Linked to type 2 diabetes (prevalence around 20%) and cardiovascular diseases, it imposes an economic burden exceeding $12 billion annually in the UAE alone. The NYUAD team's work provides a molecular lens into why fat cells malfunction, offering hope for targeted interventions.

🔬 Unraveling the Role of Nuclear Myosin 1 in Fat Cell Biology

Nuclear myosin 1 (NM1), first identified for its role in RNA polymerase I transcription and chromatin remodeling, emerges here as a master regulator during adipogenesis—the process where precursor cells (preadipocytes) differentiate into mature adipocytes (fat cells). In healthy conditions, preadipocytes shift metabolism from oxidative phosphorylation (OXPHOS, efficient energy production via mitochondria using oxygen) to aerobic glycolysis (less efficient but biosynthetic, fueling cell growth and lipid storage).72

The study demonstrates NM1 orchestrates this metabolic switch by maintaining chromatin accessibility— the openness of DNA packaging allowing transcription factors (proteins like Klf6, Foxo3) to bind enhancers near genes such as Cebpa (CCAAT/enhancer-binding protein alpha, key adipogenic transcription factor), Plin2 (perilipin 2, lipid droplet protein), and Pink1 (mitochondrial quality control). Without NM1, these pathways falter, leading to dysfunctional fat tissue.72

• NM1 binds chromatin, facilitating actomyosin contractions that expose regulatory elements.
• Deficiency downregulates adipogenic genes by 50-80% in models.
• Preserves mitochondrial function, preventing inflammatory shifts.

This chromatin-level control positions NM1 as a 'switch' toggling between healthy fat storage and pathological accumulation.

Experimental Breakthrough: From Cells to Whole-Body Models

The NYUAD team employed cutting-edge multi-omics: ATAC-seq (assay for transposase-accessible chromatin sequencing) to map open chromatin regions, and RNA-seq (RNA sequencing) to profile gene expression in NM1-knockout (KO) mouse embryonic fibroblasts (MEFs) and mesenchymal stem cells (MSCs). NM1-KO MSCs showed enlarged but immature adipocytes, impaired lipid droplet formation, and reduced differentiation efficiency.72

In vivo, NM1-deficient mice on high-fat diets developed progressive visceral obesity—excess fat around organs like the liver and intestines—unlike controls. Epididymal white adipose tissue (eWAT) analysis revealed repressed mitochondrial/adipogenic pathways and upregulated inflammation (e.g., IFNG, IL33, TNF signaling). Cross-species analysis linked NM1 to human MYO1C, suggesting translational potential.72

These rigorous models bridge cellular mechanisms to organismal phenotypes, underscoring NM1's systemic impact.

UAE's Obesity Crisis: A Call for Local Innovation

The Gulf region faces a 'diabesity' epidemic: UAE adult obesity ~35%, children 17%, diabetes 20.7%—double global averages, driven by rapid urbanization, sedentary lifestyles, and genetic predispositions.8490 Saudi Arabia and Qatar report similar rates (30-40%), costing billions in healthcare. Interventions like sugar taxes, school programs, and national guidelines exist, but molecular insights like NM1 are absent.100

NYUAD's UAE Healthy Future Study (UAEHFS), recruiting 15,000+ Emiratis, has linked genetics/lifestyle to risks, revealing high cardiometabolic factors in youth.75 This NM1 study complements it, spotlighting UAE higher education's leadership.

Photo by Muhammed Shazin on Unsplash

Spotlight on Prof. Piergiorgio Percipalle and the NYUAD Team

Leading the charge is Prof. Piergiorgio Percipalle, Associate Professor of Biology at NYUAD's Center for Genomics and Systems Biology (CGSB). With a PhD from SISSA Italy and prior roles at Karolinska Institute, his lab deciphers nuclear actomyosin in gene regulation, metabolism, and disease.114 Co-first authors Samira Khalaji and Tomas Venit, alongside Zuzana Lukáčová and Valentina Fambri, drove the work, supported by NYUAD Core Technology Platforms.

Percipalle's prior studies linked NM1 to OXPHOS protection against tumorigenesis, building to this obesity focus.140 Their interdisciplinary approach exemplifies NYUAD's global research ethos.

NYU Abu Dhabi's Ecosystem Fueling Metabolic Research

NYUAD's CGSB integrates genomics, bioinformatics, and biology, fostering breakthroughs amid UAE's health priorities. The UAEHFS provides Emirati cohorts for validation, while collaborations with Tamkeen and DOH-Abu Dhabi amplify impact.104

Recent NYUAD findings include oral microbiome-obesity links (Cell Reports, Jan 2026), where obese Emiratis show pro-inflammatory bacteria.73 Khalifa University complements with anti-obesity events, but NYUAD leads mechanistic depth.

Toward Therapies: Targeting NM1 for Metabolic Health

While preclinical, NM1 modulation—via small molecules enhancing chromatin motor activity or gene therapy restoring expression—holds promise. Previous NM1 work suggests tumor suppression via OXPHOS; here, it prevents adipose inflammation.124 Human MYO1C homology implies druggability, potentially synergizing with GLP-1 agonists like semaglutide dominant in UAE clinics.

• Enhance NM1 to boost healthy adipogenesis, reducing visceral fat.
• Combine with lifestyle interventions for UAE nationals.
• Screening for NM1 variants in high-risk populations.

Challenges: Tissue-specific delivery, off-target effects. Future trials could leverage UAEHFS biobanks.

Broader Impacts and Regional Collaboration

This research aligns with UAE's Centennial 2071 vision for health innovation, positioning universities as hubs. Gulf-wide, obesity interventions lag; NYUAD's findings could inspire Qatar/Saudi studies. For academics, it underscores chromatin regulators in non-cancer metabolism.94

Stakeholders—from policymakers to clinicians—gain actionable insights: Prioritize molecular screening in national programs.

Photo by Zalfa Imani on Unsplash

Future Horizons: From Bench to UAE Bedside

Next steps include human adipose biopsies from UAEHFS, NM1-MYO1C GWAS, and pharmacological screens. NYUAD plans collaborations with Khalifa University for translation. Globally, amid 1B obese adults projected by 2030, NM1 therapies could transform management.72

For UAE youth (17% obese), early interventions targeting metabolic switches offer prevention. Researchers worldwide eye NYUAD's model: Liberal arts fostering rigorous science.

In summary, NYU Abu Dhabi's NM1 discovery illuminates obesity's molecular roots, empowering UAE higher education to lead solutions. Explore careers in this dynamic field via higher-ed jobs, university jobs, or rate your professors. Stay informed with higher ed career advice.