On October 8, Rockefeller colleagues from labs, administrative offices, and facilities gathered for the inaugural Community Connections Lunch Series, a new initiative hosted by the Office of University Life and Community Engagement (OUCLE). The event transformed Kellen BioLink into a lively dining room filled with laughter and cross-campus conversation, where guests enjoyed maple-glazed salmon, cider-brined chicken, and roasted squash with quinoa and harvest vegetables. “This is the first time we’ve offered an event of this style for staff,” said Ashton Murray, vice president for University Life and Community Engagement. “The staff community is central to what makes Rockefeller thrive. With initiatives like this lunch series, OULCE seeks to create spaces where staff can engage thoughtfully, exchange ideas, and contribute to a culture of connection and belonging.” Learn more below.
Don't miss this piece in The Transmitter on Daniel Kronauer's latest work! His lab recently discovered that a protective screen of spurious transcriptional activity enables each olfactory neuron to express exactly one out of hundreds of olfactory receptors. “It’s a completely crazy system of transcriptional regulation—I think it’s really unprecedented," says Kronauer. "By studying such an extreme system with this expanded olfactory system, you can actually discover completely new mechanisms about very fundamental aspects of life.” Read the full article here:
Ants rely on smell to navigate nearly every aspect of their complex social lives. Thus, investigating their olfactory system, scientists believe, will reveal clues about the organization of ant society. But olfaction is one of the least understood senses across species. In ants alone, there are hundreds of lookalike odorant receptor genes that, in theory, should lead to a mish mash of mixed signals. So any attempt to understand the system has to first answer a key question: how do these insects ensure orderly processing of their most crucial sensory system? Daniel Kronauer’s lab recently uncovered the molecular safeguard that prevents olfactory chaos—a form of gene regulation that ensures each neuron activates just one receptor. The work reveals a previously unknown strategy for controlling large clusters of related genes. We asked Kronauer, head of the Laboratory of Social Evolution and Behavior, and graduate students Giacomo Glotzer and Daniel Pastor about how this finding reshapes our understanding of gene regulation in insect olfaction—and where it may ultimately lead us in the quest to understand how genes connect to behavior. Read the full Q&A below.
Bacteria have long been a key source of lifesaving antibiotics, but most species cannot be grown in the lab—leaving their therapeutic potential untapped even as multidrug resistance becomes an increasingly urgent threat. A team at Rockefeller’s Laboratory of Genetically Encoded Small Molecules recently developed a workaround to that longstanding experimental stumbling block, which could breathe new life into otherwise dry antibiotic pipelines: a method for both extracting huge stretches of bacterial DNA directly from dirt and using bioinformatics to sift antibiotics candidates out of the mix. In a recent paper, they describe how this method has already uncovered hundreds of never-before-seen genomes and two promising broad-spectrum antibiotics. The study marks a breakthrough in accessing the so-called microbial dark matter that lurks everywhere on our planet. We asked Sean F. Brady, who heads the lab, and lead author Jan Burian, how the findings may kickstart a new era of discovery in microbiology. Read the full Q&A below.
The latest issue of our research magazine Seek is out now! This edition spotlights Rockefeller’s pioneering research in infectious diseases, from taming the growing threat of vector borne disease to developing broad spectrum antivirals that could change the course of future pandemics. We also explore new strategies for long-acting HIV therapies, how AI is supercharging biomedical sciences, tech that’s changing how scientists view the brain, and more. Read the full issue here: https://bit.ly/45TEV2t
A new study from the Cao lab in Cell Reports maps—cell by cell—how caloric restriction reshapes the aging mammalian brain. The team profiled over 500,000 brain cells from mice across three ages, comparing mice on a diet versus those eating normally. They found that restricting calories curbed the age-related expansion of inflammatory cells and preserved cells that support blood vessels and myelination. It also reduced senescence-linked genes and revived circadian-clock genes, especially in ventricles and white matter. Region-specific gene programs tied to cognition and myelin maintenance were partially restored, suggesting targeted protection of brain functions. Although these findings are in mice, the integrated single-cell and spatial approach reveals concrete pathways and potential therapeutic targets for mimicking or amplifying the beneficial effects of caloric restriction to rescue brain aging. Read the full study below.
A new study from the Cao lab in Cell Reports maps—cell by cell—how caloric restriction reshapes the aging mammalian brain. The team profiled over 500,000 brain cells from mice across three ages, comparing mice on a diet versus those eating normally. They found that restricting calories curbed the age-related expansion of inflammatory cells and preserved cells that support blood vessels and myelination. It also reduced senescence-linked genes and revived circadian-clock genes, especially in ventricles and white matter. Region-specific gene programs tied to cognition and myelin maintenance were partially restored, suggesting targeted protection of brain functions. Although these findings are in mice, the integrated single-cell and spatial approach reveals concrete pathways and potential therapeutic targets for mimicking or amplifying the beneficial effects of caloric restriction to rescue brain aging. Read the full study below.
A new study from the Cao lab in Cell Reports maps—cell by cell—how caloric restriction reshapes the aging mammalian brain. The team profiled over 500,000 brain cells from mice across three ages, comparing mice on a diet versus those eating normally. They found that restricting calories curbed the age-related expansion of inflammatory cells and preserved cells that support blood vessels and myelination. It also reduced senescence-linked genes and revived circadian-clock genes, especially in ventricles and white matter. Region-specific gene programs tied to cognition and myelin maintenance were partially restored, suggesting targeted protection of brain functions. Although these findings are in mice, the integrated single-cell and spatial approach reveals concrete pathways and potential therapeutic targets for mimicking or amplifying the beneficial effects of caloric restriction to rescue brain aging. Read the full study below.
A new study from the Cao lab in Cell Reports maps—cell by cell—how caloric restriction reshapes the aging mammalian brain. The team profiled over 500,000 brain cells from mice across three ages, comparing mice on a diet versus those eating normally. They found that restricting calories curbed the age-related expansion of inflammatory cells and preserved cells that support blood vessels and myelination. It also reduced senescence-linked genes and revived circadian-clock genes, especially in ventricles and white matter. Region-specific gene programs tied to cognition and myelin maintenance were partially restored, suggesting targeted protection of brain functions. Although these findings are in mice, the integrated single-cell and spatial approach reveals concrete pathways and potential therapeutic targets for mimicking or amplifying the beneficial effects of caloric restriction to rescue brain aging. Read the full study below.
A new study from the Cao lab in Cell Reports maps—cell by cell—how caloric restriction reshapes the aging mammalian brain. The team profiled over 500,000 brain cells from mice across three ages, comparing mice on a diet versus those eating normally. They found that restricting calories curbed the age-related expansion of inflammatory cells and preserved cells that support blood vessels and myelination. It also reduced senescence-linked genes and revived circadian-clock genes, especially in ventricles and white matter. Region-specific gene programs tied to cognition and myelin maintenance were partially restored, suggesting targeted protection of brain functions. Although these findings are in mice, the integrated single-cell and spatial approach reveals concrete pathways and potential therapeutic targets for mimicking or amplifying the beneficial effects of caloric restriction to rescue brain aging. Read the full study below.
