bioRxiv Science⌕ Search

bioRxiv · 10.1101/2020.12.08.415562

Robust integrated intracellular organization of the human iPS cell: where, how much, and how variable?

Abstract

Despite the intimate link between cell organization and function, the principles underlying intracellular organization and the relation between organization, gene expression and phenotype are not well understood. We address this by creating a benchmark for mean cell organization and the natural range of cell-to-cell variation. This benchmark can be used for comparison to other normal or abnormal cell states. To do this, we developed a reproducible microscope imaging pipeline to generate a high-quality dataset of 3D, high-resolution images of over 200,000 live cells from 25 isogenic human induced pluripotent stem cell (hiPSC) lines from the Allen Cell Collection. Each line contains one fluorescently tagged protein, created via endogenous CRISPR/Cas9 gene editing, representing a key cellular structure or organelle. We used these images to develop a new multi-part and generalizable analysis approach of the locations, amounts, and variation of these 25 cellular structures. Taking an integrated approach, we found that both the extent to which a structures individual location varied ("stereotypy") and the extent to which the structure localized relative to all the other cellular structures ("concordance") were robust to a wide range of cell shape variation, from flatter to taller, smaller to larger, or less to more polarized cells. We also found that these cellular structures varied greatly in how their volumes scaled with cell and nuclear size. These analyses create a data-driven set of quantitative rules for the locations, amounts, and variation of 25 cellular structures within the hiPSC as a normal baseline for cell organization.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Viana, M. P., Chen, J., Knijnenburg, T. A., Vasan, R., Yan, C., Arakaki, J. E., Bailey, M., Berry, B., Borensztejn, A., Brown, J. M., Carlson, S., Cass, J. A., Chaudhuri, B., Cordes Metzler, K. R., Coston, M. E., Crabtree, Z. J., Davidson, S., DeLizo, C. M., Dhaka, S., Dinh, S. Q., Do, T. P., Domingus, J., Donovan-Maiye, R. M., Foster, T. J., Frick, C. L., Fujioka, G., Fuqua, M. A., Gehring, J. L., Gerbin, K. A., Grancharova, T., Gregor, B. W., Harrylock, L., Haupt, A., Hendershott, M. C., Hookway, C., Horwitz, A. R., Hughes, C., Isaac, E. J., Johnson, G. R., Kim, B., Leonard, A. N., Leung, W.. 2020-12-10. Robust integrated intracellular organization of the human iPS cell: where, how much, and how variable?. https://doi.org/10.1101/2020.12.08.415562

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↗