Search bioRxiv⌕ Search

bioRxiv · 10.1101/669713

Cell fate forecasting: a data assimilation approach to predict epithelial-mesenchymal transition

Abstract

Epithelial-mesenchymal transition (EMT) is a fundamental biological process that plays a central role in embryonic development, tissue regeneration, and cancer metastasis. Transforming growth factor-{beta} (TGF{beta}) is a major and potent inducer of this cellular transition, which is comprised of transitions from an epithelial state to an intermediate or partial EMT state, then to a mesenchymal state. Using computational models to predict state transitions in a specific experiment is inherently difficult for many reasons, including model parameter uncertainty and the error associated with experimental observations. In this study, we demonstrate that a data-assimilation approach using an ensemble Kalman filter, which combines limited noisy observations with predictions from a computational model of TGF{beta}-induced EMT, can reconstruct the cell state and predict the timing of state transitions. We used our approach in proof-of-concept \"synthetic\" in silico experiments, in which experimental observations were produced from a known computational model with the addition of noise. We mimic parameter uncertainty in in vitro experiments by incorporating model error that shifts the TGF{beta} doses associated with the state transitions. We performed synthetic experiments for a wide range of TGF{beta} doses to investigate different cell steady state conditions, and we conducted a parameter study varying several properties of the data-assimilation approach, including the time interval between observations, and incorporating multiplicative inflation, a technique to compensate for underestimation of the model uncertainty and mitigate the influence of model error. We find that cell state can be successfully reconstructed in synthetic experiments, even in the setting of model error, when experimental observations are performed at a sufficiently short time interval and incorporate multiplicative inflation. Our study demonstrates a feasible proof-of-concept for a data assimilation approach to forecasting the fate of cells undergoing EMT.\n\nAuthor summaryEpithelial-mesenchymal transition (EMT) is a biological process in which an epithelial cell loses core epithelial-like characteristics, such as tight cell-to-cell adhesion, and gains core mesenchymal-like characteristics, such as an increase in cell motility. EMT is a multistep process, in which the cell undergoes transitions from epithelial state to a partial or intermediate state, and then from a partial state to a mesenchymal state. In this study, we apply data assimilation to improve prediction of these state transitions. Data assimilation is an approach well known in the weather forecasting community, in which experimental observations are iteratively combined with predictions from a dynamical model to provide an improved estimation of both observed and unobserved system states. We show that this data assimilation approach can reconstruct cell state measurements and predict state transition dynamics using noisy observations, while minimizing the error produced by the limitations and imperfections of the dynamical model.

Source connections

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Mendez, M. J., Hoffman, M. J., Cherry, E. M., Lemmon, C. A., Weinberg, S. H.. 2019-06-12. Cell fate forecasting: a data assimilation approach to predict epithelial-mesenchymal transition. https://doi.org/10.1101/669713

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

KEEP EXPLORING

Related preprints

Sequential pathways preserve kinetochore integrity in meiosis

Kinetochores connect chromosomes to spindle microtubules, but how their integrity is maintained as they are remodelled during meiosis remains poorly understood. Here, we identify three distinct pathways linking centromeric chromatin to the outer kinetochore in budding yeast, mediated by the Ctf19 complex (Ctf19cCCAN), Mif2CENP-C and binding of Okp1CENP-Q-Ame1CENP-U to the Cse4CENP-A essential N-terminal domain (END). Although partially redundant during mitosis, all three connections are required during meiosis, with distinct temporal requirements. The assembled Ctf19cCCAN and Mif2CENP-C-dependent pathways maintain kinetochore integrity from meiotic entry, while Cse4CENP-A-Okp1CENP-Q-Ame1CENP-U binding becomes critical during prophase and the meiotic divisions. We further show that Ipl1Aurora B maintains kinetochore integrity independently of Ctf19cCCAN and provide evidence for an outer kinetochore-associated Ipl1Aurora B pool. Strikingly, Cse4CENP-A phosphomimetic mutations that restore kinetochore integrity upon Ipl1Aurora B depletion instead exacerbate defects in cells lacking Ctf19cCCAN. Our findings suggest that phosphorylation of the Cse4CENP-A N-terminal domain (NTD) by Ipl1Aurora B may regulate the use of alternative centromere-kinetochore connections to adapt to the changing requirements of meiosis.

cell biology↗

Endothelial Cell Specific Thioredoxin 1-Dependent Signaling in Oxygen-1 Induced Retinopathy

Purpose: Retinopathy of prematurity (ROP) is a leading cause of childhood blindness, characterized byoxidative stress and dysregulated angiogenesis in preterm infants with immature antioxidant systems.This study aimed to investigate the specific role of endothelial cell-specific thioredoxin 1 (TXN1), a crucial oxidoreductase, in oxygen-induced retinopathy, hypothesizing that the absence of endothelial TXN1 directly impairs angiogenesis and exacerbates hyperoxia-induced injury. Methods: We generated tamoxifen-inducible, endothelial cell-specific Txn1 knockout mice (Txn1-iECKO) and utilized the oxygen-induced retinopathy (OIR) model, exposing litters to 85% oxygen from postnatal day 7 (P7) to P12. Retinal vascular morphology during vaso-obliteration and neovascularization phases, endothelial cell proliferation, and apoptotic cell death were assessed. Furthermore, human retinal microvascular endothelial cells (HRMECs) with TXN1 knockdown were subjected to hyperoxic conditions, followed by comprehensive gene expression profiling using RT2 Profiler PCR arrays and Ingenuity Pathway Analysis. Results: Deletion of endothelial Txn1 significantly enhanced vascular regression during the hyperoxic vaso-obliteration phase at P12 and markedly exacerbated pathological neovascularization at P17. Txn1-deficient retinas exhibited significantly impaired endothelial cell proliferation during the vaso-obliteration phase, while apoptotic cell death remained unchanged. Transcriptomic analysis of TXN1-deficient HRMECs under hyperoxia revealed an enhanced activation of NRF2-mediated oxidative stress response pathways. Conclusions: These findings identify endothelial TXN1 as an essential and oxygen-dependent regulator of vascular development in ischemic retinopathy, primarily influencing endothelial proliferation and redox signaling. This suggests TXN1's crucial protective role and highlights its therapeutic potential to mitigate ROP progression by modulating endothelial cell responses to oxidative stress.

cell biology↗

A Dynamic Stem Cell State Links Environmental Cues to Skeletal and Regenerative Fates

Stem cells faithfully generate tissue architecture during development, yet how their identity and regenerative output are reshaped as anatomical niches mature and environmental signals change with aging and injury remains poorly understood. Rare skeletal stem cells (SSCs) across diverse skeletal sites are defined by combinations of cell-surface markers, precluding their genetic interrogation in vivo. Here, using spatially informed single cell transcriptomics, we identify Pannexin-3 (Panx3) to mark a dynamic functional state within bona fide SSCs and establish Panx3-CreERT2 mice for its longitudinal interrogation. Panx3 SSCs exhibit long-term clonal persistence, self-renewal and multipotency, whereas Panx3- SSCs can acquire this state. Successive SSC cohorts engage the Panx3 state during skeletal development, osteoanabolic stimulation expands pre-existing Panx3 SSC clones and injury induces it locally in previously unlabeled progenitors. Thus, anatomically distinct progenitors can converge on a common stem cell state in response to different environmental inputs. Three-dimensional reconstruction of chondrogenic niches further identifies signals that redirect Panx3-lineage cells towards stable cartilage, enabling durable regeneration in aged and osteoarthritic joints and with human SSCs. These findings establish anatomical origin, stem cell state and lineage fate as separable dimensions of stem cell identity and provide genetic access for interrogating and directing endogenous SSC function.

cell biology↗