Trophectoderm biogenesis in the preimplantation mouse embryo

Fleming, Tom P.

doi:10.1007/978-94-011-2354-9_4

Cited by 53 publications

(63 citation statements)

References 101 publications

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“…Morphologically 'mature' desmosomes, as determined by electron microscopy, are first observed in the trophectoderm (TE) layer of blastocysts at E3.5 (Collins et al, 1995;Ducibella et al, 1975;Fleming et al, 1991;Fleming et al, 1993;Fleming et al, 1994;Jackson et al, 1980) (for a review, see Cheng et al, 2005). At this stage of development, the mouse embryo consists of two cell types: the inner cell mass (ICM) that will later develop into the embryo (embryo proper); and the TE, which forms the outer cell layer of the blastocyst-stage embryo.…”

Section: Dsc3 and Desmosomes In The Blastocystmentioning

confidence: 99%

Desmocollin 3 is required for pre-implantation development of the mouse embryo

Den

Cheng

Merched-Sauvage

et al. 2006

Journal of Cell Science

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Desmocollin 3 (Dsc3) is a transmembrane glycoprotein that belongs to the cadherin family of cell adhesion receptors. Together with desmoglein(s), it forms the transmembrane core of desmosomes, a multiprotein complex involved in cell adhesion, organization of the cytoskeleton, cell sorting and cell signaling. Previous reports have suggested that Dsc3 synthesis is largely restricted to stratified epithelia, and that it plays a role in the proper differentiation of these tissues during mammalian embryonic development. To test these hypotheses, we generated Dsc3-null mice. Unexpectedly, homozygous mutants show a pre-implantation lethal phenotype. In fact, most mutants die even before mature desmosomes are formed in the embryo, suggesting a new and unexpected role of Dsc3 during early development.

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Section: Dsc3 and Desmosomes In The Blastocystmentioning

confidence: 99%

Desmocollin 3 is required for pre-implantation development of the mouse embryo

Den

Cheng

Merched-Sauvage

et al. 2006

Journal of Cell Science

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“…Desmosomal adhesion may also be compromised in invading and metastasising transitional cell carcinomas, leading to speculation regarding possible tumour suppressor function of desmosomal attachment (Tselepis et al, 1998). DMs are formed later than adherens junctions during embryogenesis (Fleming et al, 1991) but their biological importance is underlined by the embryonic lethal mouse knockouts of the desmosomal components plakoglobin (Bierkamp et al, 1996;Ruiz et al, 1996) and desmoplakin (Dp) (Gallicano et al, 1998). Recently evidence has emerged demonstrating the importance of DMs in epithelial morphogenesis and cell positioning (Runswick et al, 2001;Vasioukhin et al, 2001).…”

Section: Introductionmentioning

confidence: 99%

Lack of plakophilin 1 increases keratinocyte migration and reduces desmosome stability

South

Wan

Stone

et al. 2003

Journal of Cell Science

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Ablation of the desmosomal plaque component plakophilin 1 underlies the autosomal recessive genodermatosis, skin fragility-ectodermal dysplasia syndrome (OMIM 604536). Skin from affected patients is thickened with increased scale, and there is loss of adhesion between adjacent keratinocytes,which exhibit few small, poorly formed desmosomes. To investigate further the influence of plakophilin 1 on keratinocyte adhesion and desmosome morphology,we compared plakophilin 1-deficient keratinocytes (vector controls) with those expressing recombinant plakophilin 1 introduced by retroviral transduction. We found that plakophilin 1 increases desmosomal protein content within the cell rather than enhancing transcriptional levels of desmosomal genes. Re-expression of plakophilin 1 in null cells retards cell migration but does not alter keratinocyte cell growth. Confluent sheets of plakophilin 1-deficient keratinocytes display fewer calcium-independent desmosomes than do plakophilin 1-deficient keratinocytes expressing recombinant plakophilin 1 or keratinocytes expressing endogenous plakophilin 1. In addition electron microscopy studies show that re-expression of plakophilin 1 affects desmosome size and number. Collectively, these results demonstrate that restoration of plakophilin 1 function in our culture system influences the transition of desmosomes from a calcium-dependent to a calcium-independent state and this correlates with altered keratinocyte migration in response to wounding. Thus,plakophilin 1 has a key role in increasing desmosomal protein content, in desmosome assembly, and in regulating cell migration.

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“…The biogenesis of TJ requires the activities of aPKC: aPKCδ and ζ  are required for the localization of ZO-2 but only aPKCζ is involved in the localization of ZO-1α + (Eckert et al, 2005). The desmosomes are observed by electron microscopy at the 16-cell stage onward (Fleming et al, 1991). At the molecular level, the plakoglobin is present at the 16-cell stage while desmoplakin, desmoglein and desmocollin are detected only when the cavity forms (Fleming et al, 1991).…”

Section: 13) Establishment and Maintenance Of The Epithelial Fatementioning

confidence: 99%

“…The desmosomes are observed by electron microscopy at the 16-cell stage onward (Fleming et al, 1991). At the molecular level, the plakoglobin is present at the 16-cell stage while desmoplakin, desmoglein and desmocollin are detected only when the cavity forms (Fleming et al, 1991). Moreover, the epithelial phenotype is repressed in inner blastomeres: it has been shown that inside cells can differentiate as epithelial cells as soon as they are exposed to asymmetrical cell contacts, without synthesis of new mRNAs, demonstrating that they contain a store of untranslated mRNAs coding for all the proteins required for epithelial differentiation (Johnson, 1979) ; Louvet-Vallée et al, 2001;Spindle, 1978) If the determination of the ICM and TE fate depends on the position of the blastomeres, the maintenance of these fates require mainly the expression of two transcription factors Cdx2 and Oct4.…”

Section: 13) Establishment and Maintenance Of The Epithelial Fatementioning

confidence: 99%