Tissue-specific, temporal changes in cell adhesion to echinonectin in the sea urchin embryo

Burdsal, Carol A.; Alliegro, Mark C.; McClay, David R.

doi:10.1016/0012-1606(91)90425-3

Cited by 33 publications

(24 citation statements)

References 35 publications

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“…We eschewed enzyme-based assays (e.g. Chiarugi et al, 2000) in favor of a mechanical assay loosely based upon Burdsal et al (Burdsal et al, 1991), because the EF seemed likely to provide a mechanical deadhesion stimulus during migration. Our assay, measuring cells' centrifugal de-adhesion from upside-down coverslips, corroborated the visual impression; that is, cells that appeared flatter, with a larger footprint, better resisted de-adhesion (Fig.…”

Section: Resultsmentioning

confidence: 99%

“…In the centrifugation assay, reminiscent of Burdsal et al (Burdsal et al, 1991), coverslips were centrifuged (10 minutes; Sorvall RC5-B) cell side down on a rubber stopper in a tube filled with Dulbecco's modified Eagle's medium and fixed with formaldehyde, and the remaining adherent cells were counted in four microscope fields (two experiments).…”

Section: Methodsmentioning

confidence: 99%

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Roles of microtubules, cell polarity and adhesion in electric-field-mediated motility of 3T3 fibroblasts

Finkelstein

Chang

Chao

et al. 2004

Journal of Cell Science

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Direct-current electric fields mediate motility (galvanotaxis) of many cell types. In 3T3 fibroblasts, electric fields increased the proportion, speed and cathodal directionality of motile cells. Analogous to fibroblasts' spontaneous migration, we initially hypothesized that reorientation of microtubule components modulates galvanotaxis. However, cells with intact microtubules did not reorient them in the field and cells without microtubules still migrated, albeit slowly, thus disproving the hypothesis. We next proposed that, in monolayers wounded and placed in an electric field, reorientation of microtubule organizing centers and stable, detyrosinated microtubules towards the wound edge is necessary and/or sufficient for migration. This hypothesis was negated because field exposure mediated migration of unoriented, cathode-facing cells and curtailed migration of oriented, anode-facing cells. This led us to propose that ablating microtubule detyrosination would not affect galvanotaxis. Surprisingly, preventing microtubule detyrosination increased motility speed, suggesting that detyrosination inhibits galvanotaxis. Microtubules might enhance adhesion/de-adhesion remodeling during galvanotaxis; thus, electric fields might more effectively mediate motility of cells poorly or dynamically attached to substrata. Consistent with this hypothesis, incompletely spread cells migrated more rapidly than fully spread cells. Also, overexpression of PAK4, a Cdc42-activated kinase that decreases adhesion, enhanced galvanotaxis speed, whereas its lack decreased speed. Thus, electric fields mediate fibroblast migration via participation of microtubules and adhesive components, but their participation differs from that during spontaneous motility.

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Section: Resultsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Roles of microtubules, cell polarity and adhesion in electric-field-mediated motility of 3T3 fibroblasts

Finkelstein

Chang

Chao

et al. 2004

Journal of Cell Science

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“…Prior to ingression, PMCs are attached to each other by apical tight junctions (Balinsky, 1959) and to the hyalin layer covering the apical face of the epithelium (Katow and Solursh, 1980). At the time of ingression, PMCs lose their affinity for hyalin and echinonectin in this extra-embryonic matrix and for other cells of the blastular epithelia and gain affinity for fibronectin, which is found in the basal matrix layer (Burdsal et al, 1991;Fink and McClay, 1985;McClay and Fink, 1982). PMCs, but not their non-ingressing neighbors, constrict their apices, narrow their neck, and expand their basal ends, becoming 'bottle cells'.…”

Section: Morphogenesis Of Pmcs During Ingressionmentioning

confidence: 99%

Mechanisms, mechanics and function of epithelial–mesenchymal transitions in early development

Shook

Keller

2003

Mechanisms of Development

502

428

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Epithelial-mesenchymal transitions (EMTs) are an important mechanism for reorganizing germ layers and tissues during embryonic development. They have both a morphogenic function in shaping the embryo and a patterning function in bringing about new juxtapositions of tissues, which allow further inductive patterning events to occur [Genesis 28 (2000) 23]. Whereas the mechanics of EMT in cultured cells is relatively well understood [reviewed in Biochem. Pharmacol. 60 (2000) 1091; Cell 105 (2001) 425; Bioessays 23 (2001) 912], surprisingly little is known about EMTs during embryonic development [reviewed in Acta Anat. 154 (1995) 8], and nowhere is the entire process well characterized within a single species. Embryonic (developmental) EMTs have properties that are not seen or are not obvious in culture systems or cancer cells. Developmental EMTs are part of a specific differentiative path and occur at a particular time and place. In some types of embryos, a relatively intact epithelium must be maintained while some of its cells de-epithelialize during EMT. In most cases de-epithelialization (loss of apical junctions) must occur in an orderly, patterned fashion in order that the proper morphogenesis results. Interestingly, we find that de-epithelialization is not always necessarily tightly coupled to the expression of mesenchymal phenotypes.Developmental EMTs are multi-step processes, though the interdependence and obligate order of the steps is not clear. The particulars of the process vary between tissues, species, and specific embryonic context. We will focus on 'primary' developmental EMTs, which are those occurring in the initial epiblast or embryonic epithelium. 'Secondary' developmental EMT events are those occurring in epithelial tissues that have reassembled within the embryo from mesenchymal cells. We will review and compare a number of primary EMT events from across the metazoans, and point out some of the many open questions that remain in this field.

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“…TGF-b1 in particular is considered to be a prototypic inducer of EMT and regulates this process both during development and in adult disease states (Zavadil and Bottinger 2005;Willis and Borok 2007). Repression of E-cadherin expression is a key step in the EMT process (Burdsal et al 1991). Growth factor signalling pathways have been shown to modulate activity of transcription factors that repress E-cadherin gene expression (Thiery 2003).…”

Section: Bmp4 Induces An Epithelial -Mesenchymal Transition-like Respmentioning

confidence: 99%

BMP4 induces an epithelial–mesenchymal transition-like response in adult airway epithelial cells

et al. 2008

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Tissue-specific, temporal changes in cell adhesion to echinonectin in the sea urchin embryo

Cited by 33 publications

References 35 publications

Roles of microtubules, cell polarity and adhesion in electric-field-mediated motility of 3T3 fibroblasts

Roles of microtubules, cell polarity and adhesion in electric-field-mediated motility of 3T3 fibroblasts

Mechanisms, mechanics and function of epithelial–mesenchymal transitions in early development

BMP4 induces an epithelial–mesenchymal transition-like response in adult airway epithelial cells

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