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Back to Parsimonious Latents: Learning Task-Centric World Models from Visual Foundations

arXiv:2605.25620v1 Announce Type: new Abstract: World models enable agents to predict future dynamics conditioned on actions, making the choice of latent representation central to planning and control. Such representations are often either learned directly from pixels with limited semantic structure or inherited from frozen visual foundation models with excessive task-irrelevant detail, yielding state spaces that are poorly matched to downstream planning and control. This is especially challenging in reward-free offline settings, where the model must learn from fixed trajectories without reward supervision or online interaction. To address this, we propose TC-WM, a framework for turning foundation-model embeddings into compact, task-sufficient world representations. The key design is to treat the pretrained embedding space as a semantic scaffold rather than as the final state space: TC-WM linearly projects high-dimensional visual embeddings into a compact latent as the dynamic space, aligns a subspace with the agent's physical state via contrastive learning, and reconstructs embeddings to preserve useful visual structure. This combines the generality of foundation features with the controllability of task-centric dynamics. Theoretically, we show that TC-WM suffices to identify the underlying task-centric latent factors up to a simple transformation. Empirically, TC-WM enables test-time planning across diverse environments (e.g., Robomimic and D4RL), achieving better world-modeling quality and more precise control than state-of-the-art approaches.

Human pancreatic progenitor organoids define genetic and epigenetic barriers to early PDAC transformation

Dev Cell. 2026 May 19:S1534-5807(26)00159-0. doi: 10.1016/j.devcel.2026.04.012. Online ahead of print.

ABSTRACT

The lack of accurate human models that recapitulate pancreatic ductal adenocarcinoma (PDAC) initiation has hindered therapeutic development. Using pluripotent stem cell-derived pancreatic progenitor organoids, we established a human PDAC model that faithfully reproduces the genetic, epigenetic, and transcriptomic trajectories of tumor initiation and progression, validated against clinical datasets and tumor histopathology. We demonstrate that CDKN2A loss, which is nearly universal in patients but dispensable in mouse models, is essential for neoplastic transformation when combined with KRAS and TP53 mutations, whereas SMAD4 loss promotes tumor progression. Multi-omics profiling reveals epigenetic repression of the pancreatic lineage program during PDAC initiation, alongside AP-1-driven chromatin remodeling. We identify TET1 suppression as a mechanistic link between oncogenic ERK signaling and hypermethylation of essential pancreatic transcription factors. This model captures genetic and epigenetic determinants of human PDAC, reveals antagonism between oncogenic and lineage restriction programs, and supports TET-based lineage restoration as a potential early intervention strategy.

PMID:42161274 | PMC:PMC13196429 | DOI:10.1016/j.devcel.2026.04.012

De novo design of quasisymmetric two-component protein cages

Nature, Published online: 20 May 2026; doi:10.1038/s41586-026-10464-0

Researchers designed two-component proteins forming quasisymmetric cages via geometric frustration, enabling tunable virus-like assemblies for cargo delivery, cellular uptake and studying intracellular diffusion and protein localization.
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