Yue Wan, A*STAR, Singapore 

Cells have evolved mechanisms to respond to and recover from environmental stress.  During stress, mRNAs are transiently condensed into stress granules (SGs) and subsequently released upon stress resolution. Recent studies suggest that nonspecific trans RNA-RNA interactions drive SG assembly, however, the RNA structural landscape and RNA-RNA interactions within SGs have remained largely unexplored. Here, we employed complementary RNA structure probing approaches to directly characterize RNA conformation within SGs. Surprisingly, although cellular RNAs become globally more structured during stress, RNAs enriched in SGs are more single-stranded both intra- and intermolecularly. We further demonstrate that increased RNA single-strandedness play a role in promoting SG condensation, a process potentially mediated by RNA binding proteins, such as SRSF1. Moreover, we observed active RNA unwinding within SGs by helicases and found that depletion of the RNA helicase, DDX3X, enhances RNA pairing and reduces SG assembly. Together, our findings reveal multiple mechanisms that preserve RNA single-strandedness within SGs, and establish RNA structure regulation as a fundamental determinant of cellular plasticity during stress response 

Jun-An Chen, IMB, Academia Sinica 

TBA

Hsiu-Chuan Lin, Centre for Genomic Regulation, Barcelona, Spain

Human cells can be engineered in vitro from induced pluripotent stem cells (iPSCs) into diverse cell types and increasingly refined cellular subtypes, with broad applications in human biology, disease modelling, therapeutic screening, and cell replacement therapy. However, precise engineering of cell identity remains challenging. Many strategies still rely heavily on empirical optimization of differentiation protocols or transcription factor cocktails, while the possible design space of regulatory combinations, timing, dosage, and cellular context is too large to explore exhaustively by trial and error.

In this talk, I will discuss how single-cell genomics coupled with perturbation screening can accelerate human cell fate engineering and help move the field from empirical optimization towards a more systematic, design-driven framework. I will present our recent work showing how single-cell atlases can define target cell identities, how data-driven regulatory inference can prioritize candidate fate regulators and narrow the engineering design space, and how scalable single-cell perturbation screens can establish their causal effects. By coupling genetic and signaling perturbations with single-cell readouts, we can systematically explore cell identity landscapes and uncover how regulatory programs and signaling cues shape cell fate decisions. I will discuss how this framework enables rapid exploration of diverse phenotypic landscape of cell identities, identifies key regulatory features, and provides actionable principles for the rational design of future cell fate engineering.

Steve Mao, Editor-in-Chief, Cancer Cell

In this talk, I will explore Cancer Cell’s vision to unify foundational cancer science and clinical oncology, accelerating progress where lab insights meet real-world patient impact. Learn how we integrate cutting-edge technologies (AI, multi-omics, etc.) and systemic perspectives to decode cancer’s complexity, prioritize clinical relevance, and dismantle silos between disciplines. I’ll share how we empower scientists to publish transformative work—amplifying research through rigorous yet collaborative peer review, designed to refine ideas while fostering dialogue. Whether you’re a basic scientist, clinician, or translational researcher, discover how Cancer Cell’s supportive ecosystem elevates your work, drives global collaboration, and ultimately transforms patient outcomes.