Motion sensing superpixels (MOSES) is a systematic computational framework to quantify and discover cellular motion phenotypes.

Felix Y Zhou,Jens Rittscher,Richard P Owen,Carlos Ruiz-Puig,Michael J White,Xin Lu

doi:10.7554/elife.40162

Abstract

Correct cell/cell interactions and motion dynamics are fundamental in tissue homeostasis, and defects in these cellular processes cause diseases. Therefore, there is strong interest in identifying factors, including drug candidates that affect cell/cell interactions and motion dynamics. However, existing quantitative tools for systematically interrogating complex motion phenotypes in timelapse datasets are limited. We present Motion Sensing Superpixels (MOSES), a computational framework that measures and characterises biological motion with a unique superpixel 'mesh' formulation. Using published datasets, MOSES demonstrates single-cell tracking capability and more advanced population quantification than Particle Image Velocimetry approaches. From > 190 co-culture videos, MOSES motion-mapped the interactions between human esophageal squamous epithelial and columnar cells mimicking the esophageal squamous-columnar junction, a site where Barrett's esophagus and esophageal adenocarcinoma often arise clinically. MOSES is a powerful tool that will facilitate unbiased, systematic analysis of cellular dynamics from high-content time-lapse imaging screens with little prior knowledge and few assumptions.

Highlights

In the development of multicellular organisms, different cell types expand and migrate to form defined organ structures
Our results demonstrate that Motion Sensing Superpixels (MOSES) robustly captures the relevant aspects of epithelial interactions and fulfils requirements for unbiased high content, comparative biological video analysis and phenotypic discovery
To model the interfaces that occur in the esophagus we used the combinations: EPC2:EPC2, EPC2:CP-A and EPC2:OE33 (Fig. 1B)

Summary

Introduction

In the development of multicellular organisms, different cell types expand and migrate to form defined organ structures. Tissue development and homeostasis require coordinated collective cellular motion. In conditions such as wound healing, immune and epithelial cells need to proliferate and migrate [1,2,3]. Deregulation of key signalling pathways in pathological conditions, including cancer, causes alterations in cellular motion properties that are critical for disease development and progression, for example leading to invasion and metastasis. Sharp boundaries separate different types of epithelia: for example between the squamous and columnar epithelia in the esophagus, cervix and anus. Disruption of these boundaries can lead to disease. Understanding how tissue dynamics relates to pathological phenotypes and how it can be affected by intrinsic and extrinsic factors is a key issue

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Results

Conclusion