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Collective Growth in a Small Cell Network.

ABSTRACT: Theoretical studies suggest that many of the emergent properties associated with multicellular systems arise already in small networks [1, 2]. However, the number of experimental models that can be used to explore collective dynamics in well-defined cell networks is still very limited. Here we focus on collective cell behavior in the female germline cyst in Drosophila melanogaster, a stereotypically wired network of 16 cells that grows by ?4 orders of magnitude with unequal distribution of volume among its constituents. We quantify multicellular growth with single-cell resolution and show that proximity to the oocyte, as defined on the network, is the principal factor that determines cell size; consequently, cells grow in groups. To rationalize this emergent pattern of cell sizes, we propose a tractable mathematical model that depends on intercellular transport on a cell lineage tree. In addition to correctly predicting the divergent pattern of cell sizes, this model reveals allometric growth of cells within the network, an emergent property of this system and a feature commonly associated with differential growth on an organismal scale [3].

SUBMITTER: Imran Alsous J

PROVIDER: S-EPMC6333208 | biostudies-literature | 2017 Sep

REPOSITORIES: biostudies-literature

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Collective Growth in a Small Cell Network.

Imran Alsous Jasmin J Villoutreix Paul P Berezhkovskii Alexander M AM Shvartsman Stanislav Y SY

Current biology : CB 20170831 17

Theoretical studies suggest that many of the emergent properties associated with multicellular systems arise already in small networks [1, 2]. However, the number of experimental models that can be used to explore collective dynamics in well-defined cell networks is still very limited. Here we focus on collective cell behavior in the female germline cyst in Drosophila melanogaster, a stereotypically wired network of 16 cells that grows by ∼4 orders of magnitude with unequal distribution of volum ...[more]

PMID: 28867205

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Project description:IntroductionTransforming growth factor beta (TGF-β) has a dual role during tumor progression, initially as a suppressor and then as a promoter. Epithelial TGF-β signaling regulates fibroblast recruitment and activation. Concurrently, TGF-β signaling in stromal fibroblasts suppresses tumorigenesis in adjacent epithelia, while its ablation potentiates tumor formation. Much is known about the contribution of TGF-β signaling to tumorigenesis, yet the role of TGF-β in epithelial-stromal migration during tumor progression is poorly understood. We hypothesize that TGF-β is a critical regulator of tumor-stromal interactions that promote mammary tumor cell migration and invasion.MethodsFluorescently labeled murine mammary carcinoma cells, isolated from either MMTV-PyVmT transforming growth factor-beta receptor II knockout (TβRII KO) or TβRIIfl/fl control mice, were combined with mammary fibroblasts and xenografted onto the chicken embryo chorioallantoic membrane. These combinatorial xenografts were used as a model to study epithelial-stromal crosstalk. Intravital imaging of migration was monitored ex ovo, and metastasis was investigated in ovo. Epithelial RNA from in ovo tumors was isolated by laser capture microdissection and analyzed to identify gene expression changes in response to TGF-β signaling loss.ResultsIntravital microscopy of xenografts revealed that mammary fibroblasts promoted two migratory phenotypes dependent on epithelial TGF-β signaling: single cell/strand migration or collective migration. At epithelial-stromal boundaries, single cell/strand migration of TβRIIfl/fl carcinoma cells was characterized by expression of α-smooth muscle actin and vimentin, while collective migration of TβRII KO carcinoma cells was identified by E-cadherin+/p120+/β-catenin+ clusters. TβRII KO tumors also exhibited a twofold greater metastasis than TβRIIfl/fl tumors, attributed to enhanced extravasation ability. In TβRII KO tumor epithelium compared with TβRIIfl/fl epithelium, Igfbp4 and Tspan13 expression was upregulated while Col1α2, Bmp7, Gng11, Vcan, Tmeff1, and Dsc2 expression was downregulated. Immunoblotting and quantitative PCR analyses on cultured cells validated these targets and correlated Tmeff1 expression with disease progression of TGF-β-insensitive mammary cancer.ConclusionFibroblast-stimulated carcinoma cells utilize TGF-β signaling to drive single cell/strand migration but migrate collectively in the absence of TGF-β signaling. These migration patterns involve the signaling regulation of several epithelial-to-mesenchymal transition pathways. Our findings concerning TGF-β signaling in epithelial-stromal interactions are important in identifying migratory mechanisms that can be targeted as recourse for breast cancer treatment.

Dataset Information

Collective Growth in a Small Cell Network.

Publications

Collective Growth in a Small Cell Network.

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