Cadherins M, 11, and 6 Expression Patterns Suggest Complementary Roles in Mouse Neuromuscular Axis Development

Padilla, Françoise; Broders, Florence; Nicolet, M.‐A.; Mège, René Marc

doi:10.1006/mcne.1998.0681

Cited by 24 publications

(27 citation statements)

References 61 publications

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“…The Cdh15 DMR (ranked 14 th ; FDR < 0.02) spans exons 10 to 12 of the Cdh15 gene (Figures 1A and 2A), which maps to distal chromosome 8 (8qE2) and encodes the M-cadherin protein, a cell-adhesion protein linked to muscle and cerebellum (Padilla et al., 1998; Rose et al., 1995). By bisulfite sequencing of exon 11, we showed that this DMR fulfills the three developmental criteria of a maternally imprinted gDMR (Figures 2B and S3B): (1) methylation acquisition in the oocyte but not in sperm, (2) maintenance of maternally methylated alleles prior to implantation, as revealed by the lack of methylated alleles in maternal-imprint free Dnmt3L-/+ blastocysts compared to wild-type blastocysts, and (3) protection of the paternally unmethylated alleles after implantation, as shown in 9.5 dpc embryos derived from C57Bl6/J and CAST/Ei strains.…”

Section: Resultsmentioning

confidence: 99%

Protection against De Novo Methylation Is Instrumental in Maintaining Parent-of-Origin Methylation Inherited from the Gametes

Proudhon¹,

Duffié²,

Ajjan³

et al. 2012

Molecular Cell

122

109

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SummaryIdentifying loci with parental differences in DNA methylation is key to unraveling parent-of-origin phenotypes. By conducting a MeDIP-Seq screen in maternal-methylation free postimplantation mouse embryos (Dnmt3L-/+), we demonstrate that maternal-specific methylation exists very scarcely at midgestation. We reveal two forms of oocyte-specific methylation inheritance: limited to preimplantation, or with longer duration, i.e. maternally imprinted loci. Transient and imprinted maternal germline DMRs (gDMRs) are indistinguishable in gametes and preimplantation embryos, however, de novo methylation of paternal alleles at implantation delineates their fates and acts as a major leveling factor of parent-inherited differences. We characterize two new imprinted gDMRs, at the Cdh15 and AK008011 loci, with tissue-specific imprinting loss, again by paternal methylation gain. Protection against demethylation after fertilization has been emphasized as instrumental in maintaining parent-of-origin methylation inherited from the gametes. Here we provide evidence that protection against de novo methylation acts as an equal major pivot, at implantation and throughout life.

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Section: Resultsmentioning

confidence: 99%

Protection against De Novo Methylation Is Instrumental in Maintaining Parent-of-Origin Methylation Inherited from the Gametes

Proudhon¹,

Duffié²,

Ajjan³

et al. 2012

Molecular Cell

122

109

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“…It is also expressed in the peripheral nervous system and, in particular, in motor and sensory axons during the period of active nerve elongation and path finding. [75, 76] CDH2 is present during neuroectoderm formation and is important for nervous system development. [77, 78] CDH2 knockout mice die on day 10 of gestation due to heart defects and malformed neural tubes, although tissue development appears normal up to this stage [79].…”

Section: The Role Of Cdh2 and Cdh11 During Development And Morphogmentioning

confidence: 99%

CDH2 and CDH11 act as regulators of stem cell fate decisions

2015

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Accumulating evidence suggests that the mechanical and biochemical signals originating from cell-cell adhesion are critical for stem cell lineage specification. In this review, we focus on the role of cadherin mediated signaling in development and stem cell differentiation, with emphasis on two well-known cadherins, cadherin-2 (CDH2) (N-cadherin) and cadherin-11 (CDH11) (OB-cadherin). We summarize the existing knowledge regarding the role of CDH2 and CDH11 during development and differentiation in vivo and in vitro. We also discuss engineering strategies to control stem cell fate decisions by fine-tuning the extent of cell-cell adhesion through surface chemistry and microtopology. These studies may be greatly facilitated by novel strategies that enable monitoring of stem cell specification in real time. We expect that better understanding of how intercellular adhesion signaling affects lineage specification may impact biomaterial and scaffold design to control stem cell fate decisions in three-dimensional context with potential implications for tissue engineering and regenerative medicine.

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“…In situ hybridization (ISH) was performed on cryosections according to Bloch-Gallego et al (1999). For the mouse Cadherin-11 subclone (Padilla et al, 1998), we linearized with HindIII (Invitrogen) enzymes and used T3 RNA polymerase (Roche, Indianapolis, IN). For the mouse Peripherin subclone, we linearized with NotI (Invitrogen) enzymes and used T7 RNA polymerase (Roche) For the mouse trio subclone, we linearized with ClaI (Invitrogen) enzymes and used T7 RNA polymerase.…”

mentioning

confidence: 99%

Trio Controls the Mature Organization of Neuronal Clusters in the Hindbrain

Backer¹,

Hidalgo‐Sánchez²,

Offner³

et al. 2007

J. Neurosci.

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During the embryonic development of the hindbrain, movements of neuronal clusters allow the formation of mature "pools", in particular for inferior olivary (ION) and facial motor (fMN) nuclei. The cellular mechanisms of neuron clustering remain uncharacterized. We report that the absence of the Rho-guanine exchange factor Trio, which can activate both RhoG and Rac1 in vivo, prevents the proper formation of ION and fMN subnuclei. Rac1, but not RhoG, appears to be a downstream actor in Trio-induced lamellation. In addition, we report that Cadherin-11 is expressed by a subset of neurons through the overall period of ION and fMN parcellations, and defects observed in trio mutant mice are located specifically in Cadherin-11-expressing regions. Moreover, endogenous Cadherin-11 is found in a complex with Trio when lamellation occurs. Altogether, those results establish a link between Trio activity, the subsequent Rac1 activation, and neuronal clusters organization, as well as a possible recruitment of the Cadherin-11 adhesive receptor to form a complex with Trio.

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Cadherins M, 11, and 6 Expression Patterns Suggest Complementary Roles in Mouse Neuromuscular Axis Development

Cited by 24 publications

References 61 publications

Protection against De Novo Methylation Is Instrumental in Maintaining Parent-of-Origin Methylation Inherited from the Gametes

Protection against De Novo Methylation Is Instrumental in Maintaining Parent-of-Origin Methylation Inherited from the Gametes

CDH2 and CDH11 act as regulators of stem cell fate decisions

Trio Controls the Mature Organization of Neuronal Clusters in the Hindbrain

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