Planar Spindle Orientation and Asymmetric Cytokinesis in the Mouse Small Intestine

Fleming, Elizabeth; Zajac, Mark; Moschenross, Darcy; Montrose, David C.; Rosenberg, Daniel W.; Cowan, Ann E.; Tirnauer, Jennifer S.

doi:10.1369/jhc.7a7234.2007

Cited by 69 publications

(75 citation statements)

References 22 publications

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“…S1A,B, S2A-D). This simple mechanism, to produce an apical/basal cleavage plane for maintaining the integrity of apical membrane structures during cell division, has also been observed in the mouse intestine in vivo (Fleming et al 2007) and in 3D cultures of Caco2 cells (Jaffe et al 2008). …”

Section: Growth Of Primary Mammary Cells In 3d Cultures Produces Acinmentioning

confidence: 71%

Regulation of transgenes in three-dimensional cultures of primary mouse mammary cells demonstrates oncogene dependence and identifies cells that survive deinduction

Jechlinger¹,

Podsypanina²,

Varmus³

2009

Genes Dev.

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The advent of targeted therapies for cancer has provoked interest in experimental models for the systematic study of oncogene dependence. To that end, we developed a three-dimensional (3D) culture system to analyze the responses of primary mouse mammary epithelial cells to the induction and deinduction of oncogenes. Mammary cells derived from normal virgin mice, or from tritransgenic mice (TetO-MYC;TetO-Kras G12D ;MMTV-rtTA) in which MYC and mutant Kras can be regulated by doxycycline, develop from single cells into polarized acini. Lumen formation occurs without apparent apoptosis, and the hollow spheres of cells enlarge by division, with metaphase plates oriented perpendicularly to the apical surface. When MYC and Kras G12D are induced, the acini enlarge and form solid, depolarized spheres. Upon deinduction of MYC and Kras G12D the solid structures regress, leaving a repolarized monolayer of viable cells. These cells display a phenotype consistent with progenitors of mammary epithelium: They exclude Hoechst dye 33342, and reform acini in 3D cultures and repopulate mammary fat pads more efficiently than cells harvested from uninduced acini. Moreover, cells in the surviving spheres retain the ability to respond to reinduction and thus may represent the type of cells that give rise to recurrent tumors.

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Section: Growth Of Primary Mammary Cells In 3d Cultures Produces Acinmentioning

confidence: 71%

Regulation of transgenes in three-dimensional cultures of primary mouse mammary cells demonstrates oncogene dependence and identifies cells that survive deinduction

Jechlinger¹,

Podsypanina²,

Varmus³

2009

Genes Dev.

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“…as in vivo in mouse intestine (Fleming et al, 2007;Jinguji and Ishikawa, 1992) and vertebrate neuroepithelium (Das et al, 2003;Dubreuil et al, 2007;Kosodo et al, 2004). More recently, asymmetric furrowing has also been observed in Drosophila ovary follicular epithelium (Morais-de-Sá and Sunkel, 2013a), embryo ectoderm (Guillot and Lecuit, 2013a) and pupal notum (Founounou et al, 2013;Herszterg et al, 2013).…”

Section: Box 1 Brief Overview Of Cytokinesismentioning

confidence: 86%

Epithelial cell division – multiplying without losing touch

Bras

Borgne

2014

Journal of Cell Science

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Epithelia are compact tissues comprising juxtaposed cells that function as mechanical and chemical barriers between the body and the environment. This barrier relies, in part, on adhesive contacts within adherens junctions, which are formed and stabilized by Ecadherin and catenin proteins linked to the actomyosin cytoskeleton. During development and throughout adult life, epithelia are continuously growing or regenerating, largely as a result of cell division. Although persistence of adherens junctions is needed for epithelial integrity, these junctions are continually remodelled during cell division. In this Commentary, we will focus on cytokinesis, the final step of mitosis, a multiparty phenomenon in which the adherens junction belt plays an essential role and during which a new cell-cell interface is generated between daughter cells. This new interface is the site of intense remodelling, where new adhesive contacts are assembled and cell polarity is transmitted from mother to daughter cells, ultimately becoming the site of cell signalling.

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“…In vertebrates, spindle orientation is coordinated with cell polarity (Chang et al, 2007;Fleming et al, 2007;Konno et al, 2008;Lamprecht et al, 1986;Lechler and Fuchs, 2005;Yingling et al, 2008), as in C. elegans and Drosophila. Likewise, regulators of heterotrimeric G proteins have been shown to mediate spindle orientation during asymmetric divisions in birds and mammals (Morin et al, 2007;Sanada and Tsai, 2005).…”

Section: Discussionmentioning

confidence: 99%

Cortical domain correction repositions the polarity boundary to match the cytokinesis furrow in C. elegans embryos

et al. 2010

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SUMMARYIn asymmetrically dividing cells, a failure to coordinate cell polarity with the site of cell division can lead to cell fate transformations and tumorigenesis. Cell polarity in C. elegans embryos is defined by PAR proteins, which occupy reciprocal halves of the cell cortex. During asymmetric division, the boundary between the anterior and posterior PAR domains precisely matches the site of cell division, ensuring exclusive segregation of cell fate. The PAR domains determine the site of cell division by positioning the mitotic spindle, suggesting one means by which cell polarity and cell division might be coordinated. Here, we report that cell polarity and cell division are coordinated through an additional mechanism: the site of cell division repositions the PAR-2 boundary. G-mediated microtubule-cortex interactions appear to direct cortical flows of PAR-2 and myosin toward the site of cell division, which acts as a PAR-2 and myosin sink. Embryos with defects in PAR-2 boundary correction undergo mis-segregation of cortical polarity and cytoplasmic determinants, suggesting that PAR domain correction might help prevent cell fate transformation.

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Planar Spindle Orientation and Asymmetric Cytokinesis in the Mouse Small Intestine

Cited by 69 publications

References 22 publications

Regulation of transgenes in three-dimensional cultures of primary mouse mammary cells demonstrates oncogene dependence and identifies cells that survive deinduction

Regulation of transgenes in three-dimensional cultures of primary mouse mammary cells demonstrates oncogene dependence and identifies cells that survive deinduction

Epithelial cell division – multiplying without losing touch

Cortical domain correction repositions the polarity boundary to match the cytokinesis furrow in C. elegans embryos

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