Cell Fusions in the Developing Epithelia of C. elegans

Podbilewicz, Benjamin; White, John

doi:10.1006/dbio.1994.1041

Cited by 182 publications

(235 citation statements)

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“…The pattern of DLG-1 expression highly resembles that of the adherens junction protein AJM-1, which encodes the MH27 antigen and was previously known as JAM-1 (Kö ppen et Mohler et al, 1998;Podbilewicz and White, 1994;Priess and Hirsh, 1986;Raich et al, 1999;Wood, 1988). Indeed, DLG-1 colocalizes with AJM-1::GFP as evidenced by immunostaining (Figure 2A-F, n ϭ 18/18).…”

Section: Dlg-1 Is Required For Adherens Junction Assembly But Is Not mentioning

confidence: 91%

DLG-1 Is a MAGUK Similar to SAP97 and Is Required for Adherens Junction Formation

Firestein¹,

Rongo

2001

MBoC

117

118

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Cellular junctions are critical for intercellular communication and for the assembly of cells into tissues. Cell junctions often consist of tight junctions, which form a permeability barrier and prevent the diffusion of lipids and proteins between cell compartments, and adherens junctions, which control the adhesion of cells and link cortical actin filaments to attachment sites on the plasma membrane. Proper tight junction formation and cell polarity require the function of membrane-associated guanylate kinases (MAGUKs) that contain the PDZ protein-protein interaction domain. In contrast, less is known about how adherens junctions are assembled. Here we describe how the PDZ-containing protein DLG-1 is required for the proper formation and function of adherens junctions in Caenorhabditis elegans. DLG-1 is a MAGUK protein that is most similar in sequence to mammalian SAP97, which is found at both synapses of the CNS, as well as at cell junctions of epithelia. DLG-1 is localized to adherens junctions, and DLG-1 localization is mediated by an amino-terminal domain shared with SAP97 but not found in other MAGUK family members. DLG-1 recruits other proteins and signaling molecules to adherens junctions, while embryos that lack DLG-1 fail to recruit the proteins AJM-1 and CPI-1 to adherens junctions. DLG-1 is required for the proper organization of the actin cytoskeleton and for the morphological elongation of embryos. In contrast to other proteins that have been observed to affect adherens junction assembly and function, DLG-1 is not required to maintain cell polarity. Our results suggest a new function for MAGUK proteins distinct from their role in cell polarity. INTRODUCTIONCell adhesion facilitates the assembly of individual cells into organized tissues, and several different cell adhesion mechanisms fulfill this role (Gumbiner, 1996). One of these adhesion mechanisms is the formation of the tight junction or zonula occludens, which functions to regulate the permeability of the cell layer and to polarize the cell surface into apical and basolateral compartments (Mitic and Anderson, 1998). Tight junctions (in vertebrates) and septate junctions (in invertebrates) maintain the separation between the apical and basolateral surfaces by hindering the diffusion of lipids and proteins (Powell, 1981;Gumbiner, 1987). In contrast to tight junctions, a second mechanism of cell adhesion is the adherens junction, which is responsible for maintaining adhesion between neighboring cells and is important for intercellular communication (Muller, 2000;Vasioukhin and Fuchs, 2001).While many proteins have important roles in assembling these junctions, mutations in these proteins result in large defects in cell polarity as well. For example, mutations in the Drosophila genes bazooka (baz), crumbs (crb), discs lost (dlt), scribble (scrib), lethal (1) discs large (dlg), and lethal giant larvae (lgl), and the Caenorhabditis elegans gene let-413 disrupt epithelial cell polarity and prevent the formation of cell junctions (Legouis et al., 20...

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Section: Dlg-1 Is Required For Adherens Junction Assembly But Is Not mentioning

confidence: 91%

DLG-1 Is a MAGUK Similar to SAP97 and Is Required for Adherens Junction Formation

Firestein¹,

Rongo

2001

MBoC

117

118

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“…Staging was confirmed based on the morphology of seam hypodermal cells, which are actively dividing and migrating during L1 (Austin and Kenyon, 1994;Podbilewicz and White, 1994;Sulston and Horvitz, 1977).…”

Section: Staging Of Larvaementioning

confidence: 99%

A non-cell-autonomous role for Ras signaling inC. elegansneuroblast delamination

Parry

Sundaram

2014

Development

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Receptor tyrosine kinase (RTK) signaling through Ras influences many aspects of normal cell behavior, including epithelial-tomesenchymal transition, and aberrant signaling promotes both tumorigenesis and metastasis. Although many such effects are cellautonomous, here we show a non-cell-autonomous role for RTK-Ras signaling in the delamination of a neuroblast from an epithelial organ. The C. elegans renal-like excretory organ is initially composed of three unicellular epithelial tubes, namely the canal, duct and G1 pore cells; however, the G1 cell later delaminates from the excretory system to become a neuroblast and is replaced by the G2 cell. G1 delamination and G2 intercalation involve cytoskeletal remodeling, interconversion of autocellular and intercellular junctions and migration over a luminal extracellular matrix, followed by G1 junction loss. LET-23/EGFR and SOS-1, an exchange factor for Ras, are required for G1 junction loss but not for initial cytoskeletal or junction remodeling. Surprisingly, expression of activated LET-60/ Ras in the neighboring duct cell, but not in the G1 or G2 cells, is sufficient to rescue sos-1 delamination defects, revealing that Ras acts non-cell-autonomously to permit G1 delamination. We suggest that, similarly, oncogenic mutations in cells within a tumor might help create a microenvironment that is permissive for other cells to detach and ultimately metastasize.

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“…Second, ablation of the daughters of P5.p and P7.p VPCs in lin-11 mutant animals did not alter the invagination defect of P6.p progeny, suggesting that the effects on 1°l ineage are not an indirect consequence of the 2°lineage defect. To analyze the defects in lin-11 mutant vulval cells further, we used the ajm-1::GFP cell-junction marker (formerly known as MH27::GFP and jam-1::GFP) that reveals cell boundaries and allows the in vivo study of cell fusion events (Podbilewicz and White, 1994;Mohler et al, 1998;Raich et al, 1999). Sharma-Kishore et al have used the marker to describe the process of wild-type vulval development (Sharma-Kishore et al, 1999).…”

Section: Lin-11 Mutant Vulval Cells Exhibit Abnormal Cell Fusionsmentioning

confidence: 99%

The C. elegans LIM homeobox gene lin-11 specifies multiple cell fates during vulval development

2003

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LIM homeobox family members regulate a variety of cell fate choices during animal development. In C. elegans, mutations in the LIM homeobox gene lin-11 have previously been shown to alter the cell division pattern of a subset of the 2° lineage vulval cells. We demonstrate multiple functions of lin-11 during vulval development. We examined the fate of vulval cells in lin-11 mutant animals using five cellular markers and found that lin-11 is necessary for the patterning of both 1°and 2° lineage cells. In the absence of lin-11 function, vulval cells fail to acquire correct identity and inappropriately fuse with each other. The expression pattern of lin-11 reveals dynamic changes during development. Using a temporally controlled overexpression system, we show that lin-11 is initially required in vulval cells for establishing the correct invagination pattern. This process involves asymmetric expression of lin-11 in the 2° lineage cells. Using a conditional RNAi approach, we show that lin-11 regulates vulval morphogenesis. Finally, we show that LDB-1, a NLI/Ldb1/CLIM2 family member,interacts physically with LIN-11, and is necessary for vulval morphogenesis. Together, these findings demonstrate that temporal regulation of lin-11 is crucial for the wild-type vulval patterning.

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Cell Fusions in the Developing Epithelia of C. elegans

Cited by 182 publications

References 0 publications

DLG-1 Is a MAGUK Similar to SAP97 and Is Required for Adherens Junction Formation

DLG-1 Is a MAGUK Similar to SAP97 and Is Required for Adherens Junction Formation

A non-cell-autonomous role for Ras signaling inC. elegansneuroblast delamination

The C. elegans LIM homeobox gene lin-11 specifies multiple cell fates during vulval development

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