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Osteoclasts are bone degrading cells, notorious for their role in osteoporosis (a bone disease characterized by decreased density and structural deterioration). However, complete absence of osteoclast activity can be lethal, and optimal bone health relies on remodeling, where osteoclasts resorb old bone and osteoblasts rebuild it. Osteoclasts are large multinucleated cells that form through cell-cell fusion of their precursors. This fusion process is crucial for osteoclast differentiation, but it is not completely understood. New insights into this process could enable development of advanced pharmaceuticals that can fine-tune osteoclast activity. Using mutants derived from a lethal genetic bone disease, we discovered a unique phenotype: osteoclasts that never stop fusing, creating huge cells that are also paradoxically inactive in resorbing bone. I will discuss the genes involved, and our recent results and hypotheses about this intriguing molecular mechanism.

Fundamental understanding of physiological processes that occur at biological membranes, such as membrane fusion, necessitates addressing not only the biochemical aspects, but also biophysical aspects such as membrane tension and curvature. In this talk, I will show how we combine membrane model systems, micropipette aspiration, optical tweezers, and confocal fluorescence microscopy to study membrane shaping and remodelling. I will describe a tool we developed in which membrane bilayers are formed on polystyrene microspheres that can be trapped and manipulated with optical tweezers and brought into contact with micropipette-aspirated vesicles. Using this system, we demonstrated that membrane tension inhibits hemifusion by increasing the energy barrier for stalk formation. (Shendrik et al 2023). We then extended the approach to interact supported membranes with asymmetric GUVs, revealing a preferred direction for fusion in asymmetric membranes (Shendrik et al 2025). Expanding our understanding of how membrane tension affects membrane organization, we also explored the effect of membrane stretching on phase-separated membranes (Perlman-Illouz et al 2026). Finally, I will show how biomimetic models can be used to gain mechanistic insight into the action mechanisms of viral fusion proteins (Yosibash I. et al 2025). Together, these studies demonstrate how combining mechanical tools with biomimetic models advances our mechanistic understanding of cell membranes. FOR THE LATEST UPDATES AND CONTENT ON SOFT MATTER AND BIOLOGICAL PHYSICS AT THE WEIZMANN, VISIT OUR WEBSITE: https://www.bio

In multiclass classification with bandit feedback, a learner only observes whether its predicted label was correct, rather than the true label itself.  This simple change turns a basic supervised learning problem into a much harder exploration problem: how can one learn accurately over a large set of possible labels while receiving only minimal feedback?  In this talk, I will discuss a recent line of work studying the statistical complexity of bandit multiclass classification.  Perhaps surprisingly, we show that bandit feedback can be essentially free: with the right exploration strategy, one can match the full-information sample complexity rates up to logarithmic factors. The key technical ingredient is a new algorithmic approach to low-variance exploration that scales with the sparsity of the rewards, rather than with their ambient dimension.  Beyond resolving a substantial gap in prior work, these ideas also extend naturally to richer prediction problems such as list classification, combinatorial feedback models, and contextual bandits; somewhat unexpectedly, they have also played a role in resolving the tight sample complexity of standard full-information multiclass classification.

Based on joint work with PhD student Liad Erez and collaborators Fan Chen, Alon Cohen, Steve Hanneke, Yishay Mansour, Shay Moran, Sasha Rakhlin, and Qian Zhang.

Floral transition is accompanied by a rapid reorganization of shoot growth and architecture. A striking feature of this transition is the sudden acceleration of apical axillary meristem (AM) initiation and branching, processes that are typically delayed during vegetative development. How flowering signals coordinate this developmental shift remains poorly understood. Using tomato, we identify a transient florigen-dependent regulatory module that promotes rapid initiation of vegetative and reproductive axillary meristems during floral transition. This branching program operates in parallel with a meristem maturation pathway, and coordination between these pathways determines inflorescence complexity and shoot architecture. Our findings reveal how systemic flowering signals are integrated with localized developmental programs to generate architectural diversity.