A growing body of research, including work from Rockefeller's own Sohail Tavazoie, suggests tumors rely on proteins and genes that are unique to the nervous system to persist in the body: While investigating colorectal cancer cells, Tavazoie spotted that metastasizing tumor cells overexpress a gene called CKB. He knew that this gene helped brain cells to survive a lack of oxygen, or hypoxia, which is common inside tumors. In work published last year, Tavazoie selectively grew pancreatic cancer cell lines that were particularly good at colonizing the liver (metastasis to the liver is especially deadly). He found that these cells overexpress a different gene, called NPTX1, that makes neurons more resilient to hypoxia. “I cannot leave neuro. It comes back and haunts me,” Tavazoie says.
Tuberculosis is both curable and preventable, yet each year, it still kills more people than any other infectious disease. Rifampicin, the main treatment for hashtag#tuberculosis, is losing ground against drug-resistant bacteria and dormant infections. But a new collaborative study between Rockefeller's Elizabeth Campbell and Jeremy Rock finds that pairing rifampicin with a second inhibitor called AAP-SO₂ turns a common resistance mutation into a vulnerability, dramatically boosting the potency of both drugs in knocking out dormant infections hiding in cell clusters. The results provide a pathway for the development of future dual-inhibitor drug strategies, and reframe TB treatment as a precision strategy that could be built around better understanding molecular bottlenecks in resistant strains. “Basic science is putting us one step ahead of bacteria,” says Campbell. “Thanks to that kind of research into TB’s transcription and genetics, we can now strategize how to prevent resistance, or even exploit resistance for the development of new therapies.”
Covering topics from osteoarthritis to neurodevelopment, the inaugural symposium of Rockefeller's Marlene Hess Center for Research on Women’s Health and Biomedicine showcased research that illuminates how biological sex shapes health and disease. “While many clinically oriented women’s health centers exist across the country, few are positioned to integrate world class basic science research to illuminate the fundamental drivers of biological sex-related health differences,” says Agata Smogorzewska, director of the center and head of the Laboratory of Genome Maintenance at Rockefeller. “We are uniquely positioned to lead this effort.”
The Stavros Niarchos Foundation (SNF) Institute for Global Infectious Disease Research at Rockefeller aims to better understand the agents that cause infectious disease and to lower barriers to treatment and prevention globally. Get a closer look at what the institute has been working on in this video featuring SNF Co-President Andreas Dracopoulos, Rockefeller President Richard P. Lifton, and Rockefeller scientists Charles M. Rice, Barry S. Coller, Elaine Fuchs, Michel C. Nussenzweig, Jeremy M. Rock, Sean F. Brady, Thomas P. Sakmar, and Paul Bieniasz.
Rockefeller's Junyue Cao has been named a Hevolution/American Federation for Aging Research New Investigator Awardee in Aging Biology and Geroscience Research! Aging is a universal process involving many changes across our organs and cell types, yet it remains unclear which ones actively drive aging. Cao’s research develops new technologies to measure changes in individual cells throughout the entire lifespan. Congratulations, Jun!
Rockefeller's Elaine Fuchs tells Knowable Magazine how animals actively reallocate their amino acid resources in times of scarcity. Her research found that when animals were deprived of serine, skin stem cells devoted less effort to making hair and instead preserved their resources. This makes sense, Fuchs says: Under stressful conditions, when animals aren’t getting enough dietary protein, “what you want is to be able to repair your wounds. You don’t really care so much about making hair.”
Elaine Fuchs, the Rebecca C. Lancefield Professor and an HHMI Investigator, has spent decades uncovering why our bodies are so good at regenerating #skin—and how we might harness that understanding to combat illness, #hairloss, and perhaps even the #aging process itself. In this Q&A, Fuchs, who heads the Robin Chemers Neustein Laboratory of Mammalian Cell Biology and Development, explains why she is so interested in diseases linked to skin stem cells, such as #psoriasis and #eczema, as well as the importance of bench to bedside translation.
Cells stop dividing when telomeres become too short to protect chromosomes, a process known as replicative senescence. But what drives it, and why cells senesce far earlier under high-oxygen conditions versus low-oxygen conditions, was not fully understood, until now. A new study from Titia de Lange's lab at Rockefeller demonstrates that replicative senescence depends entirely upon the ATM kinase, a signaling protein that responds to DNA breaks and is crucial for maintaining genomic stability. The lab also found that when oxygen levels are high, ATM becomes hyperactive, responding vigorously to DNA breaks and reducing the cell’s tolerance for short telomeres. Because most tumors experience low oxygen levels, their reduced ATM response could allow hashtag#cancer cells to tolerate very short telomeres, raising the possibility that reactivating ATM could stop tumor growth.
A new paper from Rockefeller researchers Shixin Liu and Joel Cohen reveals how key regulatory proteins work in a precise hierarchy to meticulously adjust pacing during transcription. Until now, technical hurdles prevented scientists from precisely determining how the enzyme RNA polymerase II (pol II) moves along DNA, and what governs its pauses and accelerations. Liu, an expert in single-molecule methods, realized that he could overcome these barriers only by rebuilding a mammalian transcription system in vitro, piece by piece from purified proteins, and pairing it with advanced imaging techniques and computational algorithms. The idea gained momentum through a chance encounter with Cohen at Bass Dining Commons. “We sat together, and Joel asked me if I was working on anything interesting,” Liu recalls. “I sort of pitched him this project, we started looking into it together, and we’ve been collaborating since then. I’m so glad we sat at the same table that day.” Working together, the researchers developed a platform that merges biochemistry, single-molecule imaging, and computation to reveal Pol II at work in unprecedented detail. The single-molecule platform that revealed these findings is a novel approach to studying similar processes that could have broad applications in biology.
How do ant queens get crowned? Listen to Rockefeller's Daniel Kronauer on Science Friday explain how you can take two ant eggs with the exact same genes, and one can grow up to be a queen, the other a worker.
