• Physics Core Facilities
  • Physics of Complex Systems
  • Condensed Matter Physics
  • Particle Physics and Astrophysics
  • SRITP
  • Seminars
    Date:
    11
    January, 2026
    Sunday
    Hour: 13:15-14:30

    The Clore Center for Biological Physics

    Structure in Prosody

    Prof. David Biron   |   

    Lunch at 12:45

    Prosody, by and large, is the variation in pitch, timing, and loudness that gives speech its musical quality. It is pivotal in human communication, yet its structure and meaning remain subjects of ongoing research. I will describe a data-driven model for English prosody based on large-scale analysis of spontaneous conversations. As a first step, we identified approximately 200 discernible prosodic patterns, i.e., pitch contours typically spanning 1-4 words that we view as building blocks of a prosodic vocabulary, and outlined their properties and communicative meanings. Next, we revealed a Markovian logic, akin to a syntax, affecting how these elementary building blocks concatenate into coherent utterances. We further identified distinct compound functions associated with pairs of consecutive patterns and demonstrated that this Markovian structure is significantly more prevalent in spontaneous prosody compared to scripted speech. These findings offer insights into the underlying mechanisms of conversational prosody, empirically informing and refining existing theoretical concepts in linguistics. The methodology of combining unsupervised clustering analysis of large speech datasets with careful manual annotation could guide future research aimed at refining our model and expanding it to other languages.
  • Seminars
    Date:
    13
    January, 2026
    Tuesday
    Hour: 13:15-14:30

    Special Clore Center for Biological Physics

    Network Resilience Theory of Aging

    Dr. Bnaya Gross   |   

    Lunch at 12:45

    Two major theories compete to explain the origin of aging. The first, proposed by Leo Szilard in 1959, attributes aging to DNA damage. The second, articulated by Robin Holliday in the 1980s, emphasizes epigenetic alterations. While both reveal plausible molecular origins of aging, they leave important puzzles unresolved. First, mutation and epimutation burdens increase linearly with age, whereas aging phenotypes exhibit strongly nonlinear behavior. Second, key aging phenotypes cannot be traced to specific genetic or epigenetic changes; instead, they emerge collectively from their cumulative effects on cellular function.

    In this talk, I will present a network resilience theory of aging that resolves these puzzles. Network resilience is formalized as the ability of a network to sustain its basic functions under changes in its topology and dynamical variables. Our theory conceptualizes aging as a progressive loss of network resilience as cells approach a novel critical mutation-epigenetic line. We identify two regimes of cellular stability, with young cells remaining resilient while older cells exhibit increased susceptibility. Using GTEx data and numerical simulations, we link transcriptional noise to cellular susceptibility and reproduce delayed immune activation observed in aging. Overall, our theory offers a novel perspective on aging based on resilience and critical phenomena.
  • Seminars
    Date:
    18
    January, 2026
    Sunday
    Hour: 13:15-14:15

    The Clore Center for Biological Physics

    Evolution of error correction through a need for speed

    Prof. Arvind Murugan   |   

    Lunch at 12:45

    Physicists have long viewed life as a non-equilibrium process that fights the 2nd law of thermodynamics by maintaining order. While we understand how extant biological Maxwell Demons work, much less is known about how such Demons come into existence in the first place. Using theoretical and experimental work on DNA copying machinery, we show that the commonly assumed tradeoff between speed and accuracy can be inverted: error correction can actually speed up replication. The key insight is that errors cause `stalling’, i.e., misincorporated bases slow down subsequent steps by factors up to 100,000x. Correcting errors, though costly per base, avoids these long delays and leads to faster overall replication. We support this prediction with data from a large-scale polymerase mutagenesis screen showing that faster polymerases are more accurate. We further show that analogous error-correcting mechanisms, like the dynamic instability of microtubules, can emerge during self-assembly under selection for speed alone. Our work suggests that complex, dissipative error correction can evolve more easily than assumed, as a byproduct of fast replication, even before that accuracy serves any direct function like preserving genetic information.

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