Invading, Leading and Navigating Cells in <i>Caenorhabditis elegans</i>: Insights into Cell Movement <i>in Vivo</i>

Sherwood, David R.; Plastino, Julie

doi:10.1534/genetics.117.300082

Cited by 57 publications

(48 citation statements)

References 299 publications

(393 reference statements)

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“…Cell invasion is also the first step that is activated during the formation of metastases by malignant cancer cells [1]. Anchor cell (AC) invasion in C. elegans is a genetically amenable and tractable model that has provided important insights into the molecular pathways regulating cell invasion and uncovered the molecular similarities between tumor cell and developmental cell invasion [2,3].…”

Section: Introductionmentioning

confidence: 99%

The Caenorhabditis elegans homolog of the Evi1 proto-oncogene, egl-43, coordinates G1 cell cycle arrest with pro-invasive gene expression during anchor cell invasion

et al. 2020

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Cell invasion allows cells to migrate across compartment boundaries formed by basement membranes. Aberrant cell invasion is a first step during the formation of metastases by malignant cancer cells. Anchor cell (AC) invasion in C. elegans is an excellent in vivo model to study the regulation of cell invasion during development. Here, we have examined the function of egl-43, the homolog of the human Evi1 proto-oncogene (also called MECOM), in the invading AC. egl-43 plays a dual role in this process, firstly by imposing a G1 cell cycle arrest to prevent AC proliferation, and secondly, by activating pro-invasive gene expression. We have identified the AP-1 transcription factor fos-1 and the Notch homolog lin-12 as critical egl-43 targets. A positive feedback loop between fos-1 and egl-43 induces pro-invasive gene expression in the AC, while repression of lin-12 Notch expression by egl-43 ensures the G1 cell cycle arrest necessary for invasion. Reducing lin-12 levels in egl-43 depleted animals restored the G1 arrest, while hyperactivation of lin-12 signaling in the differentiated AC was sufficient to induce proliferation. Taken together, our data have identified egl-43 Evi1 as an important factor coordinating cell invasion with cell cycle arrest.

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Section: Introductionmentioning

confidence: 99%

The Caenorhabditis elegans homolog of the Evi1 proto-oncogene, egl-43, coordinates G1 cell cycle arrest with pro-invasive gene expression during anchor cell invasion

et al. 2020

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“…HMCN assembles into a variety of track‐like structures that form directly on cells to stabilize cellular adhesions, such as neuronal‐epidermal attachments, as well as extracellular scaffolds that support germ cell differentiation. HMCN also forms tracks along basement membranes (BM) that regulate the positioning and attachment of tissues to the epidermis, including the intestine, gonad, muscle, and uterus …”

Section: Introductionmentioning

confidence: 99%

Mammalian hemicentin 1 is assembled into tracks in the extracellular matrix of multiple tissues

Lin

Pope

Sasaki

et al. 2020

Developmental Dynamics

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Background: Hemicentins (HMCNs) are a family of extracellular matrix proteins first identified in Caenorhabditis elegans, with two orthologs (HMCN1 and 2) in vertebrates. In worms, HMCN is deposited at specific sites where it forms long, fine tracks that link two tissues by connecting adjacent basement membranes (BMs). By generating CRISPR/Cas9-mediated Hmcn1 and Hmcn2 knockout mice, we tested the hypothesis that HMCNs perform similar functions in mammals.Results: Hmcn1 −/− mice were viable and fertile. Using new, knockout mousevalidated HMCN1 antibodies, HMCN1 was detected in wild-type mice as fine tracks along the BM of hair and whisker follicles, in the sclera of the eyes, and in the lumen of some lymphoid conduits. It was also observed in the mesangial matrix of the kidney glomerulus. However, HMCN1 deficiency did not affect the functions of these tissues, including adherence of coat hairs and whiskers, the sieving function of lymphoid conduits, or the immune response to injected antigens. HMCN2 deficiency did not lead to any discernible phenotypes on its own or when combined with HMCN1 deficiency.Conclusion: That Hmcn1 −/− , Hmcn2 −/− , and Hmcn1/2 double knockout mice did not display any overt phenotypes implicates compensation by other members of the fibulin family. K E Y W O R D Sbasement membrane, hair follicle, lymphoid conduits, matrix protein, sclera, whisker follicle

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“…The C. elegans pharynx is a rigid, contractile feeding apparatus largely composed of radially arranged muscle and marginal cells that form an epithelium 28 . The gonad is a flexible cylindrical reproductive organ, which is enwrapped predominantly by thin gonadal sheath cells 29 . The pharyngeal epithelium and gonadal sheath cells are both surrounded by BMs that support each organ 30 .…”

Section: Resultsmentioning

confidence: 99%

α-integrins dictate distinct modes of type IV collagen recruitment to basement membranes

Jayadev

Chi

Keeley

et al. 2019

Preprint

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Basement membranes (BMs) are cell-associated extracellular matrices that support tissue integrity, signaling, and barrier properties. Type IV collagen is critical for BM mechanical and signaling functions, yet how it is directed into BMs in vivo is unclear. Through live-cell imaging of endogenous localization, conditional knockdown, and misexpression experiments, we uncovered distinct mechanisms of integrin-mediated collagen recruitment to Caenorhabditis elegans gonadal and pharyngeal BMs. The putative laminin-binding αINA-1/βPAT-3 integrin was selectively activated in the gonad and recruited laminin, which directed moderate collagen incorporation. In contrast, the putative Arg-Gly-Asp (RGD)-binding αPAT-2/βPAT-3 integrin was activated in the pharynx and recruited high levels of collagen independent of laminin. Through an RNAi screen, we further identified the small GTPase RAP-3 (Rap1) as a pharyngeal-specific PAT-2/PAT-3 activator that modulates collagen levels. Together, these studies demonstrate that tissues can use distinct mechanisms to direct collagen incorporation into BMs to precisely control collagen levels and construct diverse BMs.

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Invading, Leading and Navigating Cells in Caenorhabditis elegans: Insights into Cell Movement in Vivo

Cited by 57 publications

References 299 publications

The Caenorhabditis elegans homolog of the Evi1 proto-oncogene, egl-43, coordinates G1 cell cycle arrest with pro-invasive gene expression during anchor cell invasion

The Caenorhabditis elegans homolog of the Evi1 proto-oncogene, egl-43, coordinates G1 cell cycle arrest with pro-invasive gene expression during anchor cell invasion

Mammalian hemicentin 1 is assembled into tracks in the extracellular matrix of multiple tissues

α-integrins dictate distinct modes of type IV collagen recruitment to basement membranes

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