Search bioRxiv⌕ Search

bioRxiv · 10.1101/2021.07.22.453371

Learning the rules of collective cell migration using deep attention networks

Abstract

Collective, coordinated cellular motions underpin key processes in all multicellular organisms, yet it has been difficult to express the rules behind these motions in clear, interpretable forms. Here we apply deep attention networks to analyze several canonical living tissues systems and present the underlying collective migration rules for each tissue type using only cell migration trajectory data. We use these networks to learn the behaviors of key tissue types with distinct collective behaviors--epithelial, endothelial, and metastatic breast cancer cells--and show how the results complement traditional biophysical approaches. In particular, we present attention maps indicating the relative influence of neighboring cells to the learned turning decisions of a focal cell. These attention networks reveal distinct patterns of influence and attention unique to each model tissue. Endothelial cells exhibit tightly focused attention on their immediate forward-most neighbors, while cells in more expansile epithelial tissues are more broadly influenced by neighbors in a relatively large forward sector. Attention maps of ensembles of more mesenchymal, metastatic cells reveal completely symmetric attention patterns, indicating the lack of any particular coordination or direction of interest. Moreover, we show how attention networks are capable of detecting and learning how these rules changes based on biophysical context, such as location within the tissue and cellular crowding. That these results require only cellular trajectories and no modeling assumptions highlights the potential of attention networks for providing further biological insights into complex cellular systems. Author SummaryCollective behaviors are crucial to the function of multicellular life, with large-scale, coordinated cell migration enabling processes spanning organ formation to coordinated skin healing. However, we lack effective tools to discover and cleanly express collective rules at the level of an individual cell. Here, we employ a carefully structured neural network to extract collective information directly from cell trajectory data. The network is trained on data from various systems, including well-studied cell types (HUVEC and MDCK cells) which display visually distinct forms of collective motion, and metastatic cancer cells (MDA-MB-231) which are highly uncoordinated. Using these trained networks, we can produce attention maps for each system, which indicate how a cell within a tissue takes in information from its surrounding neighbors, as a function of weights assigned to those neighbors. Thus for a cell type in which cells tend to follow the path of the cell in front, the attention maps will display high weights for cells spatially forward of the focal cell. We present results in terms of additional metrics, such as accuracy plots and number of interacting cells, and encourage future development of improved metrics.

Source connections

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

LaChance, J., Suh, K., Cohen, D. J.. 2021-07-22. Learning the rules of collective cell migration using deep attention networks. https://doi.org/10.1101/2021.07.22.453371

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

Three-dimensional mapping of human lung fibrosis identifies spatial coupling between tissue microarchitecture and maladaptive repair states

Human lung fibrosis progressively destroys three-dimensional tissue architecture, yet how the structural microenvironment shapes cellular states remains unclear. Integrating 3D X-ray histology with spatial omics, we generate a volumetric multimodal atlas of human lung fibrosis that enables direct interrogation of relationships between tissue microarchitecture and spatial molecular programmes. We identify collapse of the alveolar-capillary unit - the coupled loss of alveolar type 1 epithelial cells, capillary endothelial cells, and basement membrane integrity - as a structural transition associated with early fibrogenesis. Surrounding transitional zones exhibit aberrant epithelial differentiation and proteolytic matrix remodelling, with epithelium shifting toward bronchiolised, airway-like states. Stromal activation converges on spatially restricted fibrogenic cores, sites of maximal collagen maturation and matrix stabilisation that function as signalling hubs within surrounding perifocal and vascular microenvironments. Molecular signatures of atlas-defined tissue states were associated with lung function and mortality across independent patient cohorts. Together, these data support a model in which fibrosis emerges as a spatial tissue-state process, with alveolar-capillary collapse redirecting repair towards mechanically stabilised niches that reinforce pathological remodelling.

systems biology↗

A three-factor model can explain symmetry breaking and the n-1 rule during X-chromosome inactivation

X-chromosome inactivation (XCI) is a mammalian gene regulatory process that via chromosome-scale transcriptional silencing, leaves active a single X chromosome per diploid genome complement. The mechanisms that enable cells to select the appropriate number of X chromosomes to inactivate while leaving others active remain unclear. We demonstrate that all known chromosomal counting scenarios during XCI can be accounted for by a three-factor mathematical model that includes (1) Xist, the long noncoding RNA (lncRNA) responsible for gene silencing during XCI in eutherians, (2) an X-linked transcriptional activator of Xist, and (3) the autosomally-encoded SPEN, an Xist RNA-binding protein that is essential for gene silencing during XCI. In our model, symmetry between active X chromosomes is broken by stochastic differences in the number of Xist molecules that associate with the X chromosomes at the onset of XCI. Subsequently, integrated positive and negative feedback loops amplify then propagate superstoichiometric assemblies of SPEN complexed with Xist on the inactive chromosome(s), and select for levels of X-linked activator that enable only one X chromosome per diploid genome complement to remain active. Thus, asymmetric propagation of the SPEN-Xist ribonucleoprotein complex may play an essential role in symmetry breaking and chromosomal counting during XCI, independently of or in concert with cis-acting networks of DNA regulatory elements. Our results also have conceptual implications for gene regulatory circuits on autosomes.

systems biology↗

stem.MAP: Identification of cell-type-specific protein complexes in mammalian embryonic stem cells.

Protein complexes carry out critical functions during development. Mapping cell-type-specific protein complexes in early embryogenesis is essential for uncovering the molecular mechanisms of embryonic development. We unfortunately currently lack a catalog of protein complexes specific for embryogenesis including embryonic stem cells. Here we develop a proteomics-based machine learning workflow to predict protein complexes present in mouse embryonic stem cells (mESC). Our method integrates data from a cell-type agnostic protein complex resource with co-fractionation mass spectrometry (CF-MS) experiments on mESC. Our resource, stem.MAP, identifies 3,986 complexes encompassing ~133,000 unique interactions, and 8,616 proteins. stem.MAP captures variant complexes critical for stem cell function including the PRC2, BAF and NuRD complexes. stem.MAP also discriminates mutually exclusive interactions specific to embryonic stem cells (e.g. Eif4ebp2 - Eif4e). Finally we observe 1,388 high confidence stem.MAP interactions found only in mESC CF-MS data, many with support from AlphaFold modeling and a gastruloid coregulation network. We make stem.MAP protein complexes available through our web resource: stem.proteincomplexes.org. We anticipate stem.MAP will be beneficial to the study of early development and we expect our proteomics-based machine learning workflow to be applicable to the creation of any context-specific protein interaction network.

systems biology↗