Stanford Advisors


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  • Rapid coral bleaching recovery via symbiont transfer from healthy corals. Science advances Collins, D. S., Sipkova, J., Mollica, N. R., Rolander, T., Klepac, C. N., Calistro, G. F., Barone, V., Micheli, F., Palumbi, S. R. 2026; 12 (42): eaeh1580

    Abstract

    Coral bleaching, the temperature-induced loss of dinoflagellate symbionts, is a major driver of global coral reef decline. Although corals can regain symbionts through repopulation of residual symbionts or via environmental acquisition, these processes are often too slow to prevent coral mortality. Mechanisms that enable rapid and effective symbiont reintroduction leading to full recovery remain largely unknown. Here, we demonstrate coral bleaching recovery through contact-mediated transfer of symbionts from healthy corals using small coral fragments. We show that symbiont transfer is rapid, occurring over days to weeks, and highly efficient, with only brief physical contact with healthy corals required. A single week of contact, and in some cases as few as 3 days, provides sufficient symbionts to initiate sustained and full self-recovery. By 1 week, symbiont population doubling time is approximately 4 days, up to an order of magnitude faster than most recovery times for corals in the field. We identify tissue fusion as the mechanism enabling directional symbiont transfer from healthy to bleached coral tissue. As a result, contact-dependent recovery is restricted to corals of the same genet, whereas heterologous genet pairings trigger antagonistic interactions. However, symbiont transfer via polyp uptake occurs immediately upon contact in both same-genet and mixed-genet pairings, revealing an additional, slower pathway for symbiont transfer that is insufficient on its own to support colony recovery. Collectively, these findings reveal a previously unrecognized natural process for efficiently reintroducing symbionts to bleached corals, providing a foundation for research into potential recovery interventions.

    View details for DOI 10.1126/sciadv.aeh1580

    View details for PubMedID 42873873

    View details for PubMedCentralID PMC13665998

  • Characterization of cellular wound resistance in the giant ciliate Stentor coeruleus. Soft matter Paul, R., Nadkarni, A. V., Sipkova, J., Sato, J. E., Zhang, K. S., Barone, V., Marshall, W. F., Tang, S. K. 2025

    Abstract

    Resistance to mechanical stress is essential for cells to prevent wounding and maintain structural integrity. This capability is especially critical for free-living single-celled organisms, which routinely encounter mechanical stress from their natural habitats. We investigated Stentor coeruleus, a single-celled ciliate known for its remarkable wound repair capacity, as a model for studying mechanical wound resistance. While previous work focused on wound repair in Stentor, the structures that enable it to resist wounding remain poorly understood. We characterized how Stentor resisted mechanical stress during transit through a microfluidic constriction. Using high-speed imaging, we tracked the transit dynamics of the cells and linked them to wounding outcomes. Larger cells experienced longer transit times in the constriction and were more prone to rupture, often failing to recover shape due to membrane rupture and loss of cytoplasm. To elucidate the role of the Stentor cytoskeleton, we performed drug-mediated disruption of KM fibers, which are microtubule bundles in the Stentor cytoskeleton. Drug-treated cells exhibited an increased likelihood of membrane rupture at the constriction, implicating KM fibers in wound resistance. To investigate the resistance of Stentor cells to hydrodynamic stress, we injected the cells at increasing flow rates through the constriction. Interestingly, cells were more resistant to larger hydrodynamic stresses up to a threshold, potentially due to shear-thinning of the cytoplasm. Together, these results suggest that Stentor relies on both cytoskeletal architecture and cytoplasmic rheology to withstand mechanical stress, offering insights into cellular strategies for wound resistance in the absence of rigid extracellular structures.

    View details for DOI 10.1039/d5sm00643k

    View details for PubMedID 41090415