Ask any question about EPFL courses, lectures, exercises, research, news, etc. or try the example questions below.
DISCLAIMER: The Graph Chatbot is not programmed to provide explicit or categorical answers to your questions. Rather, it transforms your questions into API requests that are distributed across the various IT services officially administered by EPFL. Its purpose is solely to collect and recommend relevant references to content that you can explore to help you answer your questions.
Biological cycles such as the cell cycle and circadian rhythms are fundamental cell-autonomous processes that are often obscured in single-cell RNA sequencing (scRNA-seq) data by other sources of variation, including cell-type identity, metabolic or disease-associated states. Disentangling these continuous periodic trajectories from other forms of cellular variability remains a major challenge in single-cell analysis. Here, we introduce CoPhaser, an algorithm designed to learn context-dependent periodic manifolds that decompose scRNA-seq count data into independent periodic and non-periodic sources of variation, while maintaining interpretability of manifold coordinates across diverse biological contexts. CoPhaser employs a biologically informed variational autoencoder with a structured latent space that explicitly separates cycle phases from cellular context, while controlling their mutual information. By modeling gene expression as context-modulated harmonic functions, the model captures flexible but biologically motivated deformations of periodic manifolds. We demonstrate that CoPhaser recovers biologically accurate continuous cell-cycle phases across diverse RNA sequencing technologies, including highly heterogeneous situations such as development and cancer, without requiring prior knowledge of gene expression programs or cell-cycle states. In two cancer applications, CoPhaser reveals subtype-specific proliferation dynamics, identifying quiescent primitive states in relapsed pediatric acute myeloid leukemia and distinguishes proliferation-driven gene overexpression from constitutive overexpression to uncover potential robust therapeutic targets in triple-negative breast cancer. CoPhaser readily generalizes to other periodic systems, enabling the reconstruction of circadian clocks in the mouse aorta and the identification of cell-type and subtype-specific circadian differences. Furthermore, it maps continuous endometrial remodeling across the human menstrual cycle, uncovering distinct transcriptional dynamics between women with endometriosis and controls. Together, CoPhaser provides a versatile and interpretable framework for dissecting the interplay between cellular identity and biological cycles in single-cell data.