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Lab Reporter

Amazing Science Facts

Unlock a treasure trove of mind-blowing science facts every month with the latest issue of Lab Reporter. Dive into the wonders of the universe, explore groundbreaking discoveries, and ignite your curiosity like never before. From the mysteries of deep space to the marvels of cutting-edge technology, Lab Reporter brings you the most fascinating and inspiring stories from the world of science. Explore the intricacies of the Human Body, delve into Earth Science, uncover the secrets of Space, learn about extraordinary Animals, and stay updated with the latest in Science and Technology.

Featured Amazing Science Facts

Science and Technology

Sequence-Encoded Tubular Architectures in Spider Silk Proteins

Spider dragline silk is famous for being tougher than steel, yet it is spun from proteins that are intrinsically disordered in solution. A long-standing puzzle has been how these huge, floppy spidroins can stay soluble at extremely high concentrations in the silk gland while still being “primed” to assemble into ultra-strong fibers.

This study focuses on major ampullate spidroins (MaSp1 and MaSp2) from the black widow spider (Latrodectus hesperus). Using multiscale molecular dynamics simulations combined with small-angle X-ray scattering (SAXS) and solution NMR, the authors show that these proteins do not exist as simple random coils. Instead, they form dynamic ensembles that include a minor but crucial population of compact tubular conformers, about 3–4 nm in diameter and ~50 nm long.

These tubules are enriched in β-turns and bends, so they remain flexible locally while adopting an overall elongated, compact shape. The key design principle lies in the amphiphilic sequence patterning: hydrophobic poly(Ala) blocks alternate with more hydrophilic Gly-Gly-X motifs, driving the packing of segments into tubular architectures. Mutational simulations that disrupt this pattern weaken or eliminate the tubules, highlighting that the tubular structure is encoded directly in the amino-acid sequence.

By including a fraction of these tubules in SAXS fitting, the model finally reconciles earlier SAXS data (suggesting compact particles) with NMR data (showing high disorder and mobility). This provides the missing structural level between local disorder and macroscopic fiber formation.

The work reveals that spider silk proteins are not just shapeless chains but contain sequence-encoded, metastable tubular substructures. These transient tubules explain how spidroins can remain soluble at ~30 wt% inside the gland, yet be pre-organized for rapid, hierarchical self-assembly into some of nature’s toughest fibers. In other words, spider silk balances disorder, metastability, and structure through a clever sequence design.

Future Applications

These insights offer concrete design rules for next-generation biomaterials:

  • Using amphiphilic patterning in synthetic proteins or polymers to create self-assembling, high-strength fibers
  • Engineering recombinant silks or silk-like hydrogels that exploit metastable tubular intermediates for controlled assembly and toughness
  • Designing IDP-based nanostructures that stay soluble under processing conditions but solidify into robust materials on demand (e.g., for medical sutures, tissue scaffolds, or flexible electronics)

The study turns spider silk from a biological curiosity into a template for programmable, adaptive materials.

Sequence-Encoded Tubular Architectures in Spider Silk Proteins

Science and Technology

Target Cell Adhesion Limits Macrophage Phagocytosis and Promotes Trogocytosis

Macrophages protect us by engulfing pathogens, dying cells and even antibody-tagged cancer cells. However, they can also perform trogocytosis – a process where they “nibble” pieces from a target cell instead of swallowing it whole. What determines whether a macrophage fully eats a cell or just bites off fragments has been unclear.

In this study, researchers used model cancer cell lines and primary macrophages to dissect this decision. They triggered engulfment with two different pro-phagocytic signals: antibodies blocking the “don’t-eat-me” receptor CD47 and a HER2-specific CAR on macrophages. Surprisingly, when the target cells were strongly attached to a surface or to neighboring cells, macrophages preferentially performed trogocytosis rather than full phagocytosis – they stripped membrane and proteins, but left the target largely intact.

To test the role of adhesion, the team disrupted integrin-mediated attachment in target cells, either with an RGD peptide or by CRISPR knockout of the αV integrin subunit. This made cells less sticky and significantly increased full phagocytosis. Conversely, forcing cells to adhere more strongly by ectopically expressing E-cadherin reduced phagocytosis. Finally, they examined mitotic cells, which naturally round up and detach. Arresting cells in mitosis led to markedly higher phagocytosis, consistent with the idea that low adhesion favors complete engulfment.

The study demonstrates that target cell adhesion is a physical checkpoint that can tip macrophages from full phagocytosis toward trogocytosis. Highly adherent cancer cells are harder to “eat whole,” so macrophages end up nibbling instead, potentially allowing some cells to survive despite immune attack. By contrast, cells that are less anchored – like mitotic cells – are more easily fully engulfed.

These findings suggest several routes to improve macrophage-based cancer immunotherapies:

  • Combining pro-phagocytic agents (e.g., anti-CD47) with drugs that reduce tumor cell adhesion (targeting integrins or cadherins) to convert nibbling into efficient clearance
  • Designing CAR-macrophage therapies that exploit phases when tumor cells are naturally less adherent (e.g., during mitosis) to maximize killing
  • Using trogocytosis readouts as a biomarker of how “protected” tumor cells are by their mechanical and adhesive environment, guiding combination treatment strategies

In essence, the work shows that fighting cancer is not only about biochemical signals, but also about the mechanics of how tightly a cell holds on to its surroundings.

Target Cell Adhesion Limits Macrophage Phagocytosis and Promotes Trogocytosis