The role of cadherins during primordial germ cell migration and early gonad formation in the mouse

Bendel-Stenzel, Michael; Gomperts, Miranda; Anderson, Rebecca Cogwell; Heasman, Janet; Wylie, Christopher

doi:10.1016/s0925-4773(99)00287-7

Cited by 139 publications

(126 citation statements)

References 31 publications

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“…This network becomes progressively aggregated into clusters of cells towards the end of migration. Antibodies against E-cadherin blocked the process of PGC aggregation in cultured embryo slices and prevented PGCs from forming tight clusters at the genital ridges (Bendel-Stenzel et al, 2000).…”

Section: How Do Pgcs Find Their Targets? Mousementioning

confidence: 97%

Primordial germ cell migration

Molyneaux¹,

Wylie²

2004

Int. J. Dev. Biol.

Self Cite

222

159

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Mutational and antisense screens in Drosophila and zebrafish, and transcriptional profiling and time-lapse analysis in the mouse, have contributed greatly to our understanding of PGC development. In all three systems, the behavior of PGCs is controlled by growth factors which signal through G-protein coupled receptors and/or tyrosine kinase receptors. Additionally, regulated cell-cell and cell-substrate adhesion is important for PGC motility. Finally, localized growth factors may control PGC survival and consequently PGC position. Chemotaxis, regulated adhesion and cell survival are important for multiple migration processes which occur during development and disease. PGC migration shares these features.

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Section: How Do Pgcs Find Their Targets? Mousementioning

confidence: 97%

Primordial germ cell migration

Molyneaux¹,

Wylie²

2004

Int. J. Dev. Biol.

Self Cite

222

159

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“…Corresponding receptors CXCL4 and C-KIT (KIT oncoprotein) are expressed by the PGCs (Molyneaux et al 2001, 2003, Stebler et al 2004, Farini et al 2007). The adherens junction component E-cadherin and b1-integrin, expressed by PGCs as they migrate out of the hindgut, are necessary for their colonization of the genital ridges; E-cadherin is responsible for germ cell-germ cell interactions, while b1-integrin is likely to facilitate interactions of germ cells with the extracellular matrix (Anderson et al 1999, Bendel-Stenzel et al 2000. SDF1 and KITL are thought to act also as survival factors during migration , Molyneaux et al 2003, Runyan et al 2006.…”

Section: Migration Of the Pgcsmentioning

confidence: 99%

Sex determination in mammalian germ cells: extrinsic versus intrinsic factors

Bowles

Koopman²

2010

Reproduction

109

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Mammalian germ cells do not determine their sexual fate based on their XX or XY chromosomal constitution. Instead, sexual fate is dependent on the gonadal environment in which they develop. In a fetal testis, germ cells commit to the spermatogenic programme of development during fetal life, although they do not enter meiosis until puberty. In a fetal ovary, germ cells commit to oogenesis by entering prophase of meiosis I. Although it was believed previously that germ cells are pre-programmed to enter meiosis unless they are actively prevented from doing so, recent results indicate that meiosis is triggered by a signaling molecule, retinoic acid (RA). Meiosis is avoided in the fetal testis because a male-specifically expressed enzyme actively degrades RA during the critical time period. Additional extrinsic factors are likely to influence sexual fate of the germ cells, and in particular, we postulate that an additional male-specific fate-determining factor or factors is involved. The full complement of intrinsic factors that underlie the competence of gonadal germ cells to respond to RA and other extrinsic factors is yet to be defined.

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“…Homophilic E-Cadherin binding between adjacent cells has been shown to elicit signal transduction simply by engaging the extracellular domains of cadherins (Liu et al, 2006;Perrais et al, 2007). Additionally, as with the Ecad ⌬/⌬ mutants, blocking of Cadherin binding might also decrease cell to cell contact in wild-type NSCs (Bendel-Stenzel et al, 2000).…”

Section: Disruption Of E-cadherin Adhesion Reduces Nsc Self-renewal Imentioning

confidence: 99%

E-Cadherin Regulates Neural Stem Cell Self-Renewal

Karpowicz¹,

Willaime‐Morawek²,

Balenci³

et al. 2009

J. Neurosci.

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E-Cadherin, a cell adhesion protein, has been shown to take part in the compartmentalization, proliferation, survival, and differentiation of cells. E-Cadherin is expressed in the adult and embryonic forebrain germinal zones in vivo, and in clonal colonies of cells derived from these regions and grown in vitro. Mice carrying E-Cadherin floxed genes crossed to mice expressing Cre under the Nestin promoter demonstrate defects in the self-renewal of neural stem cells both in vivo and in vitro. The functional role of E-Cadherin is further demonstrated using adhesion-blocking antibodies in vitro, which specifically target cadherin extracellular adhesive domains. Adult neural stem cell colonies decrease in the presence of E-Cadherin antibodies in a dosage-dependent manner, in contrast to P-Cadherin antibody. On overexpression of normal E-Cadherin and a mutated E-Cadherin, containing no intracellular binding domain, an increased number of clonal adult neural stem cell colonies are observed. These data suggest it is specifically E-Cadherin adhesion that is responsible for these self-renewal effects. These data show the importance of E-Cadherin in the neural stem cell niche and suggest E-Cadherin regulates the number of these cells.

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The role of cadherins during primordial germ cell migration and early gonad formation in the mouse

Cited by 139 publications

References 31 publications

Primordial germ cell migration

Primordial germ cell migration

Sex determination in mammalian germ cells: extrinsic versus intrinsic factors

E-Cadherin Regulates Neural Stem Cell Self-Renewal

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