We are transforming the marine animal Hydractinia symbiolongicarpus into a powerful "organismal factory" for biological discovery. While many model organisms are hard to work with, Hydractinia is genetically flexible and easy to handle. Hydractinia already have a strong foundation of data, including a complete map of its genome and a detailed atlas of its cell types. Now, we are building advanced tools to manipulate this system. Our lab focuses on developing and refining CRISPR-Cas9 gene editing, precise base editing, and glowing protein markers (luciferase-fluorescence). These tools allow us to visualize and control life at the molecular level, creating a versatile platform for genetic engineering.
Our next focus addresses a critical medical challenge: Cancer Stem Cells (CSCs). These are the cells responsible for tumors returning after treatment because they possess "stemness"—the ability to copy themselves endlessly and turn into different cell types. To stop cancer, we must understand the "switch" that controls this ability. Since this is hard to study in humans, we use Hydractinia which naturally keeps its stem cells active for its whole life. We are investigating how the cell’s energy and food intake (metabolism) controls this switch. Specifically, we are looking at the cell's massive hunger for DNA building blocks (nucleotides) and proteins during rapid growth, aiming to find a way to starve CSCs and shut down their ability to regenerate.
Coral reefs, the rainforests of the ocean, exist because of a partnership (symbiosis) between animals (Cnidarians) and tiny algae (Alveolates). We want to understand how this relationship works by recreating it in the lab. Using Hydractinia—a close cousin of coral—we are studying how it interacts with various partners, including algae, bacteria, and fungi. By teasing apart these complex interactions in a controlled environment, we aim to uncover the fundamental rules of how different species live together, which is crucial for understanding ecosystem health and the biology of infection.
Beyond marine life, we are exploring how chemical marks on DNA help bacteria survive and become dangerous. We focus on a specific mark called 6mA (and its RNA cousin, m6A). Originally found in bacteria, 6mA acts like a traffic signal that controls when DNA is copied and helps the cell identify which DNA strand to repair. We believe these chemical signals play a major role in how bacteria like Salmonella survive stress and evolve resistance to antibiotics. By mapping this relationship, we hope to understand how "superbugs" persist and find new targets to stop them.
2025
David & Helen, ... Febrimarsa ... , Uri Frank, Jordi Solana. The Hydractinia cell atlas reveals cellular and molecular principles of cnidarian coloniality . Nature Comm. link
2023
Febrimarsa, ... , Uri Frank. Random incorporated N6‐methyldeoxyadenosine delays zygotic transcription initiation in a cnidarian. EMBO Journal. link
Koto, Tetsuo, ... , Febrimarsa, ..., Uri Frank, Oleg Simakov. Chromosome-level genome assembly of Hydractinia symbiolongicarpus. G3. link
Miguel, Febrimarsa, ... , Uri Frank. Senescence induced cellular reprogramming drives cnidarian whole-body regeneration. Cell Reports. link
Anna, ... Febrimarsa ... , Uri Frank, Andrew Flaus. Hydrozoan sperm-specific SPKK motif-containing histone H2B variants stabilise chromatin with limited compaction. Development. Link
2020
Timothy, ... Febrimarsa ..., Uri Frank. Transcription factor ap2 controls cnidarian germ cell induction. Science. Link
2015
Sebastian, Febrimarsa, ..., Ross Waller. Endosymbiosis undone by stepwise elimination of the plastid in parasitic dinoflagellates. PNAS. Link