Cell polarity

Romereim, Sarah M.; Dudley, Andrew T.

doi:10.4161/org.7.3.18583

Cited by 20 publications

(14 citation statements)

References 105 publications

(151 reference statements)

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“…The MD mesenchyme-specific expression of Wnt5A and MD epithelium-specific expression of Wnt7A adds further complexity to the respective roles in uterine development (Mericskay 2004). The different phenotypes observed by the knockout of either Wnt7a or Wnt5a suggests that these ligands have different functional roles, which might be attributable to the separate signaling pathways used by the respective ligands, i.e., the canonical β-catenin pathway for WNT7A (Mikels and Nusse 2006b) and the Ca 2+ or planar cell polarity pathway for WNT5A (Loscertales 2008; Romereim and Dudley 2011). However, WNT5A can signal through the canonical β-catenin pathway, depending on specific WNT receptor expression (He 1997; Mikels and Nusse 2006a; van Amerongen 2012).…”

Section: Introductionmentioning

confidence: 99%

Induction of WNT inhibitory factor 1 expression by Müllerian inhibiting substance/antiMullerian hormone in the Müllerian duct mesenchyme is linked to Müllerian duct regression

Park

Tanaka

Arango

et al. 2014

Developmental Biology

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A key event during mammalian sexual development is regression of the Müllerian ducts (MDs) in the bipotential urogenital ridges (UGRs) of fetal males, which is caused by the expression of Müllerian inhibiting substance (MIS) in the Sertoli cells of the differentiating testes. The paracrine signaling mechanisms involved in MD regression are not completely understood, particularly since the receptor for MIS, MISR2, is expressed in the mesenchyme surrounding the MD, but regression occurs in both the epithelium and mesenchyme. Microarray analysis comparing MIS signaling competent and Misr2 knockout embryonic UGRs was performed to identify secreted factors that might be important for MIS-mediated regression of the MD. A seven-fold increase in the expression of Wif1, an inhibitor of WNT/β-catenin signaling, was observed in the Misr2-expressing UGRs. Whole mount in situ hybridization of Wif1 revealed a spatial and temporal pattern of expression consistent with Misr2 during the window of MD regression in the mesenchyme surrounding the MD epithelium that was absent in both female UGRs and UGRs knocked out for Misr2. Knockdown of Wif1 expression in male UGRs by Wif1-specific siRNAs beginning on embryonic day 13.5 resulted in MD retention in an organ culture assay, and exposure of female UGRs to added recombinant human MIS induced Wif1 expression in the MD mesenchyme. Knockdown of Wif1 led to increased expression of β-catenin and its downstream targets TCF1/LEF1 in the MD mesenchyme and to decreased apoptosis, resulting in partial to complete retention of the MD. These results strongly suggest that WIF1 secretion by the MD mesenchyme plays a role in MD regression in fetal males.

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Section: Introductionmentioning

confidence: 99%

Induction of WNT inhibitory factor 1 expression by Müllerian inhibiting substance/antiMullerian hormone in the Müllerian duct mesenchyme is linked to Müllerian duct regression

Park

Tanaka

Arango

et al. 2014

Developmental Biology

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“…It is composed of three distinct zones—the resting zone, the proliferative zone, and the hypertrophic zone—followed by the ossification front (67, 71, 73, 119) (Figure 1). Lesser-differentiated cells in the resting zone enter the proliferative zone, where they divide perpendicular to the plane of the growth plate, intercalate over each other, and form pillars of discoid chondrocytes (73, 84, 119, 132). Eventually, the cells receive signals that promote their differentiation into hypertrophic chondrocytes, leading to a tremendous increase in cell volume.…”

Section: Overview Of Early Skeletal Development and Endochondral Ossimentioning

confidence: 99%

“…The effect of the centrosome-associated genes on stature may be due to the requirement of the centrosome to form the primary cilium, a structure necessary to maintain the organization of the growth plate (59, 119, 132). There are exceptions to these general correlations between clinical features and the type of gene mutated.…”

Section: The Primordial Dwarfismsmentioning

confidence: 99%

“…As the chondrocytes divide, the daughter cells divide perpendicular to the column and spread over one another to align within the column (84, 118a). This process, called chondrocyte rotation (132), is regulated by WNT signaling through the planar-cell polarity pathway (84, 119). Mouse models of skeletal ciliopathies have disorganized growth plates that underlie the growth insufficiency.…”

Section: The Skeletal Ciliopathiesmentioning

confidence: 99%

“…These analyses could also shed light on the potential connection between the primary cilium, planar-cell polarity, and components of the cell cycle such as ORC1 that are linked to the centrosome/primary cilium (53, 57, 133). Although there is clearly a role for both the planar-cell polarity pathway (43a, 84, 119, 147a) and the primary cilium (132) in skeletal development and growth, their functional relationship is intensely debated (12a, 147). Clearly, there is much work to be done to clarify these associations, but the data collected will certainly be of clinical and basic significance.…”

Section: The Skeletal Ciliopathiesmentioning

confidence: 99%

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Advances in Skeletal Dysplasia Genetics

Geister¹,

Camper

2015

Annu. Rev. Genom. Hum. Genet.

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Skeletal dysplasias result from disruptions in normal skeletal growth and development and are a major contributor to severe short stature. They occur in approximately 1/5,000 births, and some are lethal. Since the most recent publication of the Nosology and Classification of Genetic Skeletal Disorders, genetic causes of 56 skeletal disorders have been uncovered. This remarkable rate of discovery is largely due to the expanded use of high-throughput genomic technologies. In this review, we discuss these recent discoveries and our understanding of the molecular mechanisms behind these skeletal dysplasia phenotypes. We also cover potential therapies, unusual genetic mechanisms, and novel skeletal syndromes both with and without known genetic causes. The acceleration of skeletal dysplasia genetics is truly spectacular, and these advances hold great promise for diagnostics, risk prediction, and therapeutic design.

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Planar Cell Polarity Aligns Osteoblast Division in Response to Substrate Strain

Galea¹,

Meakin²,

Savery

et al. 2014

Journal of Bone and Mineral Research

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Exposure of bone to dynamic strain increases the rate of division of osteoblasts and also influences the directional organization of the cellular and molecular structure of the bone tissue that they produce. Here, we report that brief exposure to dynamic substrate strain (sufficient to rapidly stimulate cell division) influences the orientation of osteoblastic cell division. The initial proliferative response to strain involves canonical Wnt signaling and can be blocked by sclerostin. However, the strain-related orientation of cell division is independently influenced through the noncanonical Wnt/planar cell polarity (PCP) pathway. Blockade of Rho-associated coiled kinase (ROCK), a component of the PCP pathway, prevents strain-related orientation of division in osteoblast-like Saos-2 cells. Heterozygous loop-tail mutation of the core PCP component van Gogh-like 2 (Vangl2) in mouse osteoblasts impairs the orientation of division in response to strain. Examination of bones from Vangl2 loop-tail heterozygous mice by µCT and scanning electron microscopy reveals altered bone architecture and disorganized bone-forming surfaces. Hence, in addition to the well-accepted role of PCP involvement in response to developmental cues during skeletal morphogenesis, our data reveal that this pathway also acts postnatally, in parallel with canonical Wnt signaling, to transduce biomechanical cues into skeletal adaptive responses. The simultaneous and independent actions of these two pathways appear to influence both the rate and orientation of osteoblast division, thus fine-tuning bone architecture to meet the structural demands of functional loading. © 2014 The Authors. Journal of Bone and Mineral Research published by Wiley Periodicals, Inc. on behalf of the American Society for Bone and Mineral Research.

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Cell polarity

Cited by 20 publications

References 105 publications

Induction of WNT inhibitory factor 1 expression by Müllerian inhibiting substance/antiMullerian hormone in the Müllerian duct mesenchyme is linked to Müllerian duct regression

Induction of WNT inhibitory factor 1 expression by Müllerian inhibiting substance/antiMullerian hormone in the Müllerian duct mesenchyme is linked to Müllerian duct regression

Advances in Skeletal Dysplasia Genetics

Planar Cell Polarity Aligns Osteoblast Division in Response to Substrate Strain

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