bioRxiv Science⌕ Search

bioRxiv · 10.1101/2023.10.27.564403

Early human fetal lung atlas reveals the temporal dynamics of epithelial cell plasticity.

Abstract

While animal models have provided key insights into conserved mechanisms of how the lung forms during development, human-specific developmental mechanisms are not always captured. To fully appreciate how developmental defects and disease states alter the function of the lungs, studies in human lung models are important. Here, we sequenced >150,000 single single-cells from 19 healthy human fetal lung tissues from gestational weeks 10-19 and identified at least 58 unique cell types/states contributing to the developing lung. We captured novel dynamic developmental trajectories from various progenitor cells that give rise to club, ciliated, and pulmonary neuroendocrine cells. We also identified four CFTR-expressing progenitor cell types and pinpointed the temporal emergence of these cell types. These developmental dynamics reveal broader epithelial cell plasticity and novel lineage hierarchies that were not previously reported. Combined with spatial transcriptomics, we identified both cell autonomous and non-cell autonomous signalling pathways that may dictate the temporal and spatial emergence of cell lineages. Finally, we showed that human pluripotent stem cell-derived fetal lung models capture cell lineage trajectories specifically through CFTR-expressing progenitor cells, that were also observed in the native fetal tissue. Overall, this study provides a comprehensive single-cell atlas of the developing human lung, outlining the temporal and spatial complexities of cell lineage development. HighlightsO_LISingle-cell transcriptomics atlas from 19 human fetal lungs reveals cellular heterogeneity and previously unappreciated cellular plasticity in the epithelial compartment. C_LIO_LIIdentification of novel CFTR-expressing progenitor cells that gives rise to club, ciliated and PNEC. C_LIO_LINovel RNA velocity facilitated the identification of dynamic lineage trajectories in the epithelial compartment. C_LIO_LITemporally regulated cell signaling through promiscuous interactions between sender and receiving cells may dictate cell lineage fates. C_LIO_LIIntegration of human pluripotent stem cell (hPSC)-derived fetal lung cells and organoids with primary lung dataset show hPSC-differentiations captures key developmental trajectories of fetal epithelial cell states. C_LI

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Quach, H. T., Farrell, S., Kanagarajah, K., Wu, M., Xu, X., Kallurkar, P., Turinsky, A., Bear, C., Ratjen, F., Goyal, S., Moraes, T. J., Wong, A.. 2023-10-28. Early human fetal lung atlas reveals the temporal dynamics of epithelial cell plasticity.. https://doi.org/10.1101/2023.10.27.564403

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

KEEP EXPLORING

Related preprints

Neogenin-1 marks myeloid-primed fetal hematopoietic stem cells that undergo progressive lineage-restriction with age

During aging, hematopoietic stem cells (HSCs) increasingly shift from balanced to myeloid-biased differentiation, resulting in reduced lymphoid output and impaired adaptive immunity. The question of whether this lineage bias is established in a subset of HSCs during early development or primarily emerges with aging warrants further investigation. Here, we investigate whether myeloid-biased HSCs (my-HSCs) are established at the fetal liver stage by specifically examining Neogenin-1 (NEO1), a previously defined marker of my-HSCs. We identify two distinct populations of Hoxb5+ HSCs in the fetal liver: NEO1+ and NEO1-, with NEO1+ HSCs exhibiting transcriptional and functional characteristics consistent with my-HSCs. With age, my-HSC-associated transcriptional programs become increasingly reinforced across the Hoxb5+ pHSC compartment, with NEO1+ cells showing early enrichment of this program and both NEO1+ and NEO1- cells acquiring broader myeloid-biased features in aging. These findings suggest that lineage programming can begin early in development and is further shaped by age-related changes, potentially contributing to the functional decline observed in the aging hematopoietic system.

developmental biology↗

Distinct roles for partially redundant transcription factors in Caenorhabditis elegans mesoderm lineage development

Developmental transcription factors often have overlapping functions, making it difficult to define the distinct roles of individual factors during lineage specification. We investigated the partially redundant transcription factors TBX-35 and CEH-51 in the Caenorhabditis elegans embryonic MS mesodermal lineage using 4D lineage tracing, reporter imaging, genetics, and single-cell RNA sequencing. In tbx-35 mutants, MS descendants showed progressively slower cell cycles and a division pattern that increasingly resembled the cousin C lineage. Fate-regulator expression also shifted toward C-like features, including ectopic pal-1 and expanded HLH-1 expression, although mutant cells did not simply adopt normal C-lineage positions. Loss of tbx-35 also impaired a later MS-dependent Notch induction in the AB lineage while leaving an earlier induction intact. CEH-51 showed a different pattern of activity whereby its protein became enriched in anterior MS daughters, and ceh-51 mutants produced later, more restricted lineage defects that were strongest in descendants of cells with higher CEH-51 levels. Single-cell profiling identified overlapping but nonidentical sets of genes dependent on the two factors. TBX-35-dependent changes were strongest at earlier stages, whereas CEH-51-dependent genes became more prominent later and were enriched in anterior MS sublineages. Finally, temperature-shift experiments determined that the severity and onset of tbx-35 mutant phenotypes depend on the maternal temperature environment and cannot be explained by differences in residual CEH-51 expression. These findings reveal that TBX-35 and CEH-51 contribute differently across the MS lineage and that reliable mesoderm development is supported by overlapping zygotic and maternal regulatory inputs.

developmental biology↗

Dynamic microtubules drive yolk-cytoplasm segregation in the syncytial Drosophila embryo

Yolk-cytoplasm segregation is among the earliest spatial organization events in the developing embryo of many oviparous animals. The segregation process is intimately linked to early embryonic cleavage and pattern formation, and exhibits a wide range of spatial and temporal diversity. However, the underlying cytoskeletal mechanism remains largely unknown, except for a small number of species. Using quantitative live imaging, we investigated yolk segregation in the Drosophila embryo during the syncytial nuclear cycles 11-14. We find that the yolk vesicles move progressively inward in spatial and temporal coordination with the inward expanding microtubule networks that are nucleated from centrosomes positioned at the cortex, whereas cortical actin meshwork remains spatially restricted. Using the gnu RNAi embryo to decouple nuclear migration and division from cytoskeletal dynamics, we establish causality with targeted pharmacological disruption and find that microtubule dynamics is required for yolk segregation, while depolymerization of actin has no discernible effect. In support of a mechanism of growth-propelled passive displacement, microtubule plus end comets come in apparent contact with yolk vesicles, and injected, inert microbeads are displaced towards the embryo center presumably by the same pushing force. These findings identify microtubule polymerization as a predominant driver of yolk-cytoplasm segregation in Drosophila and suggest that diverse cytoskeletal mechanisms evolved to accomplish this crucial reorganization process

developmental biology↗