Role of gap junctions during early embryo development

Houghton, Franchesca D.

doi:10.1530/rep.1.00277

Cited by 88 publications

(78 citation statements)

References 75 publications

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“…If so, some reports about the significance of gap junctional communication should be cautiously taken. For example, during preimplantation development several connexin proteins are expressed and assembled into gap junctions in the plasma membrane at compaction but the functional significance of connexin diversity remains controversial [34]. The opinion that function of connexin is not necessary for development of primplantation embryo is mainly based on the presumption that gap junction intercellular communication can be inhibited by AGA [35].…”

Section: Discussionmentioning

confidence: 99%

“…The GJIC thus cannot be completely inhibited by AGA. Since no specific inhibitors are capable of blocking all potential channel types up to the present, it is difficult to know whether intercellular communication is dispensable for development of the preimplantation embryo [34]. Although gap junction channels are still widely considered to be large, non-specific pores connecting cells, the diversity of the connexin family led to more attention on the permeability characteristics of small molecules.…”

Section: Discussionmentioning

confidence: 99%

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Cx31 is assembled and trafficked to cell surface by ER-Golgi pathway and degraded by proteasomal or lysosomal pathways

Cai

Liu

et al. 2005

Cell Res

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Gap junctions, consisting of connexins, allow the exchange of small molecules (<1 kD) between adjacent cells, thus providing a mechanism for synchronizing the responses of groups of cells to environmental stimuli. Connexin 31 is a member of the connexin family. Mutations on connexin 31 are associated with erythrokeratodermia variabilis, hearing impairment and peripheral neuropathy. However, the pathological mechanism for connexin 31 mutants in these diseases are still unknown. In this study, we analyzed the assembly, trafficking and metabolism of connexin 31 in HeLa cells stably expressing connexin 31. Calcein transfer assay showed that calcein transfer was inhibited when cells were treated with Brefeldin A or cytochalasin D, but not when treated with nocodazole or α-glycyrrhetinic acid, suggesting that Golgi apparatus and actin filaments, but not microtubules, are crucial to the trafficking and assembly of connexin 31, as well as the formation of gap junction intercellular communication by connexin 31. Additionally, α-glycyrrhetinic acid did not effectively inhibit gap junctional intercellular communication formed by connexin 31. Pulse-chase assay revealed that connexin 31 had a half-life of about 6 h. Moreover, Western blotting and fluorescent staining demonstrated that in HeLa cells stably expressing connexin 31, the amount of connexin 31 was significantly increased after these cells were treated with proteasomal or lysosomal inhibitors. These findings indicate that connexin 31 was rapidly renewed, and possibly degraded by both proteasomal and lysosomal pathways.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Cx31 is assembled and trafficked to cell surface by ER-Golgi pathway and degraded by proteasomal or lysosomal pathways

Cai

Liu

et al. 2005

Cell Res

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“…GJ have been shown to play a basic role on embryo viability (Fleming et al, 2000); however, how they are able to regulate normal growth of the embryo remains an open question. Contrasting literature data arise on functional requirements for GJ in pre-implantation development (see Houghton, 2005 for review). In fact, GJ are established in early mouse embryo (Lo and Gilula, 1979) and it was shown that perturbation of GJ communication during the 8-16 cell stage exerted a morula decompaction, that in turn induced developmental defects (Bevilacqua et al, 1989;Becker and Davies, 1995;, although without altering blastocyst formation or a polarized allocation of cell lineages (Vance and Wiley, 1999).…”

Section: Gap Junction Channels In Embryo Developmentmentioning

confidence: 99%

Ion currents in embryo development

Tosti

Boni

Gallo

2016

Birth Defects Research Pt C

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Ion channels are proteins expressed in the plasma membrane of electrogenic cells. In the zygote and blastomeres of the developing embryo, electrical modifications result from ion currents that flow through these channels. This phenomenon implies that ion current activity exerts a specific developmental function, and plays a crucial role in signal transduction and the control of embryogenesis, from the early cleavage stages and during growth and development of the embryo. This review describes the involvement of ion currents in early embryo development, from marine invertebrates to human, focusing on the occurrence, modulation, and dynamic role of ion fluxes taking place on the zygote and blastomere plasma membrane, and at the intercellular communication between embryo cell stages.Birth Defects Research (Part C) 108:6-18, 2016.V C 2016 Wiley Periodicals, Inc.

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“…Gap junction intercellular communication (GJIC) transmits various signals including activation of the Hippo signaling pathway, which is associated with differentiation of the trophectoderm (TE) / inner cell mass (ICM) [3]. GJs have also been suggested to play a role in blastocoel formation of the preimplantation embryo [4].…”

Section: Introductionmentioning

confidence: 99%

“…Though it is expected to depend on gap junctions, pharmacologic inhibitors of GJIC have no effect on blastocyst development [12]. These discrepancies remain unresolved [4,7].…”

Section: Introductionmentioning

confidence: 99%

Dysfunction in gap junction intercellular communication induces aberrant behavior of the inner cell mass and frequent collapses of expanded blastocysts in mouse embryos

Togashi

Kumagai

Sato

et al. 2015

J Assist Reprod Genet

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Purpose We investigated the role of gap junctions (GJs) in embryological differentiation, and observed the morphological behavior of the inner cell mass (ICM) by time-lapse movie observation (TLM) with gap junction inhibitors (GJis). Methods ICR mouse embryos were exposed to two types of GJis in CZB medium: oleamide (0 to 50 μM) and 1-heptanol (0 to 10 mM). We compared the rate of blastocyst formation at embryonic day 4.5 (E4.5) with E5.5. We also observed and evaluated the times from the second cleavage to each embryonic developing stage by TLM. We investigated embryonic distribution of DNA, Nanog protein, and Connexin 43 protein with immunofluorescent staining. Results In the comparison of E4.5 with E5.5, inhibition of gap junction intercellular communication (GJIC) delayed embryonic blastocyst formation. The times from the second cleavage to blastocyst formation were significantly extended in the GJitreated embryos (control vs with oleamide, 2224±179 min vs 2354±278 min, p=0.013). Morphological differences were traced in control versus GJi-treated embryos until the hatching stage. Oleamide induced frequent severe collapses of expanded blastocysts (77.4 % versus 26.3 %, p=0.0001) and aberrant ICM divisions connected to sticky strands (74.3 % versus 5.3 %, p=0.0001). Immunofluorescent staining indicated Nanog-positive cells were distributed in each divided ICM. Conclusions GJIC plays an important role in blastocyst formation, collapses of expanded blastocysts, and the ICM construction in mouse embryos.

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Role of gap junctions during early embryo development

Cited by 88 publications

References 75 publications

Cx31 is assembled and trafficked to cell surface by ER-Golgi pathway and degraded by proteasomal or lysosomal pathways

Cx31 is assembled and trafficked to cell surface by ER-Golgi pathway and degraded by proteasomal or lysosomal pathways

Ion currents in embryo development

Dysfunction in gap junction intercellular communication induces aberrant behavior of the inner cell mass and frequent collapses of expanded blastocysts in mouse embryos

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