Extracellular matrix and cytoskeletal dynamics during branching morphogenesis

Kim, Hye Young; Nelson, Celeste M.

doi:10.4161/org.19813

Cited by 68 publications

(68 citation statements)

References 69 publications

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“…Although many studies have highlighted requirements for numerous signaling molecules and transcription factors during branching morphogenesis (Costantini and Kopan, 2010;Harunaga et al, 2011;Hauser and Hoffman, 2015;Hennighausen and Robinson, 2005;Iber and Menshykau, 2013;Kwon and Larsen, 2015;Shih et al, 2013;Varner and Nelson, 2014), it is not fully understood at the cell and tissue level how such diverse regulatory pathways orchestrate the extensive physical remodeling that shapes branched epithelial tissues. Recent advances in microscopy have established that specific dynamic cell behaviors, such as changes in cell motility, cell-cell adhesion and cell-extracellular matrix interactions, are key functional mediators of this tissue reorganization (Daley and Yamada, 2013;Friedl and Gilmour, 2009;Harunaga et al, 2011;Huebner and Ewald, 2014;Kim and Nelson, 2012;Nelson and Larsen, 2015;Varner and Nelson, 2014). However, how such dynamic cell and tissue behavior is guided by localized regulatory molecules at specific sites within a tissue remains largely unknown.…”

Section: Introductionmentioning

confidence: 99%

RETRACTED: Btbd7 is essential for region-specific epithelial cell dynamics and branching morphogenesis in vivo

et al. 2017

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Branching morphogenesis of developing organs requires coordinated but poorly understood changes in epithelial cell-cell adhesion and cell motility. We report that Btbd7 is a crucial regulator of branching morphogenesis in vivo. Btbd7 levels are elevated in peripheral cells of branching epithelial end buds, where it enhances cell motility and cellcell adhesion dynamics. Genetic ablation of Btbd7 in mice disrupts branching morphogenesis of salivary gland, lung and kidney. Btbd7 knockout results in more tightly packed outer bud cells, which display stronger E-cadherin localization, reduced cell motility and decreased dynamics of transient cell separations associated with cleft formation; inner bud cells remain unaffected. Mechanistic analyses using in vitro MDCK cells to mimic outer bud cell behavior establish that Btbd7 promotes loss of E-cadherin from cell-cell adhesions with enhanced migration and transient cell separation. Btbd7 can enhance E-cadherin ubiquitination, internalization, and degradation in MDCK and peripheral bud cells for regulating cell dynamics. These studies show how a specific regulatory molecule, Btbd7, can function at a local region of developing organs to regulate dynamics of cell adhesion and motility during epithelial branching morphogenesis.

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Section: Introductionmentioning

confidence: 99%

RETRACTED: Btbd7 is essential for region-specific epithelial cell dynamics and branching morphogenesis in vivo

et al. 2017

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“…Although they share some common structural features, each organ is characterized by a specific structure and uses distinct molecular mechanisms for branching (reviewed in REF. 49). ECM remodelling plays a crucial part in governing organ branching by providing structural integrity and regulating diverse cellular processes such as cell shape, cell motility and cell growth.…”

Section: Ecm Remodelling In Branching Morphogenesismentioning

confidence: 99%

Remodelling the extracellular matrix in development and disease

Bonnans

Chou

Werb

2014

Nat Rev Mol Cell Biol

3,327

2,877

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The extracellular matrix (ECM) is a highly dynamic structure that is present in all tissues and continuously undergoes controlled remodelling. This process involves quantitative and qualitative changes in the ECM, mediated by specific enzymes that are responsible for ECM degradation, such as metalloproteinases. The ECM interacts with cells to regulate diverse functions, including proliferation, migration and differentiation. ECM remodelling is crucial for regulating the morphogenesis of the intestine and lungs, as well as of the mammary and submandibular glands. Dysregulation of ECM composition, structure, stiffness and abundance contributes to several pathological conditions, such as fibrosis and invasive cancer. A better understanding of how the ECM regulates organ structure and function and of how ECM remodelling affects disease progression will contribute to the development of new therapeutics.

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“…Components of the ECM, including collagens, laminins, glycoproteins and proteoglycans, are essential for branching morphogenesis Pritchett et al, 2011;Kim and Nelson, 2012;Daley and Yamada, 2013). Sox9 has been reported to regulate several genes encoding ECM components (Pritchett et al, 2011).…”

Section: Roles Of Sox9 In Lacrimal Gland Branching Morphogenesismentioning

confidence: 99%

FGF signaling activates a Sox9-Sox10 pathway for the formation and branching morphogenesis of mouse ocular glands

et al. 2014

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Murine lacrimal, harderian and meibomian glands develop from the prospective conjunctival and eyelid epithelia and produce secretions that lubricate and protect the ocular surface. Sox9 expression localizes to the presumptive conjunctival epithelium as early as E11.5 and is detected in the lacrimal and harderian glands as they form. Conditional deletion showed that Sox9 is required for the development of the lacrimal and harderian glands and contributes to the formation of the meibomian glands. Sox9 regulates the expression of Sox10 to promote the formation of secretory acinar lobes in the lacrimal gland. Sox9 and FGF signaling were required for the expression of cartilageassociated extracellular matrix components during early stage lacrimal gland development. Fgfr2 deletion in the ocular surface epithelium reduced Sox9 and eliminated Sox10 expression. Sox9 deletion from the ectoderm did not affect Fgf10 expression in the adjacent mesenchyme or Fgfr2 expression in the epithelium, but appeared to reduce FGF signaling. Sox9 heterozygotes showed a haploinsufficient phenotype, in which the exorbital branch of the lacrimal gland was absent in most cases. However, enhancement of epithelial FGF signaling by expression of a constitutively active FGF receptor only partially rescued the lacrimal gland defects in Sox9 heterozygotes, suggesting a crucial role of Sox9, downstream of FGF signaling, in regulating lacrimal gland branching and differentiation.

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Extracellular matrix and cytoskeletal dynamics during branching morphogenesis

Cited by 68 publications

References 69 publications

RETRACTED: Btbd7 is essential for region-specific epithelial cell dynamics and branching morphogenesis in vivo

RETRACTED: Btbd7 is essential for region-specific epithelial cell dynamics and branching morphogenesis in vivo

Remodelling the extracellular matrix in development and disease

FGF signaling activates a Sox9-Sox10 pathway for the formation and branching morphogenesis of mouse ocular glands

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