Multiphoton imaging of chick retinal development in relation to gap junctional communication

Becker, David L.; Webb, Kevin F.; Thrasivoulou, Christopher; Lin, Chih-Chi; Nadershahi, Roxana; Tsakiri, Niki; Cook, Jeremy E.

doi:10.1113/jphysiol.2007.138776

Cited by 8 publications

(6 citation statements)

References 22 publications

(25 reference statements)

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“…Pearson et al [50]. Using a modified experimental system, it was shown that gap-junctional communication is important for the ability of progenitor cells and newborn neurons to change the direction of their movement [51]. In the case of the zebrafish retina, genetic tools can be combined with liveimaging methods.…”

Section: Retinamentioning

confidence: 99%

Interkinetic nuclear migration: beyond a hallmark of neurogenesis

Kosodo

2012

Cell. Mol. Life Sci.

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Interkinetic nuclear migration (INM) is an oscillatory nuclear movement that is synchronized with the progression of the cell cycle. The efforts of several researchers, following the first report of INM in 1935, have revealed many of the molecular mechanisms of this fascinating phenomenon linking the timing of the cell cycle and nuclear positioning in tissue. Researchers are now faced with a more fundamental question: is INM important for tissue, particularly brain, development? In this review, I summarize the current understanding of the regulatory mechanisms governing INM, investigations involving several different tissues and species, and possible explanations for how nuclear movement affects cell-fate determination and tissue formation.

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Section: Retinamentioning

confidence: 99%

Interkinetic nuclear migration: beyond a hallmark of neurogenesis

Kosodo

2012

Cell. Mol. Life Sci.

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“…The movement of Cx43 puncta in the cell body shows strong correlation with the nuclear translocation, implying the association with the centrosome and a potential role of Cx43 in nuclear translocation. This is coincident with the involvement of Cx43 in the interkinetic nuclear migration in chick retina development (Becker, D. 2007). The above studies on neuronal migration seem to support a role of Cx43 in the locomotion machinery of the neurons.…”

Section: Cell Migration Is a Common Phenomenon During Development Andsupporting

confidence: 73%

A descriptive and functional study of zebrafish Connexin43

Zhang

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Connexin43(Cx43) encodes a gap junction protein. Cx43 is specifically expressed in blood vessel endothelial cells in the zebrafish embryo as demonstrated by in situ hybridization. When Cx43 is knocked down with antisense morpholinos, the zebrafish embryos have defects in the intersegmental vessel branching and vascular perfusion. These phenotypes reflect problems in endothelial cell migration. Further analysis with microangiography revealed that the endothelial tubes or lumens fail to form normally. The co-injection of Cx43 morpholinos and p53 morpholinos rescued the vascular defects to limited degrees. The co-injection of Cx43 morpholinos with VE-Cadherin morpholino enhanced the effects observed with the injection of Cx43 morpholino alone. The transgenic zebrafish expressing the fusion protein of Cx43 and egfp under control of flk1 promoter (Tg[flk1: Cx43-egfp]) has been generated for studying the dynamic regulation of Cx43 protein in zebrafish endothelium. From live imaging of this transgenic line, green fluorescent puncta from Cx43-gfp can be found in the endothelial cells. Those puncta could be patches of gap junctional channels or undocked hemichannels on the cell-to-cell borders. The existence of hemichannels could support a role of Cx43 in cue sensing for migration or in the endothelial lumen formation. Immunohistochemistry of VE-Cadherin in Tg[flk1: Cx43-egfp] line shows that not all the Cx43-egfp puncta are co-localized with the VE-Cadherin. The endogenous Cx43 appears on the putative surface of the endothelial cells of the sprouting intersegmental vessels at 22 hours post fertilization (hpf), as determined by staining with an antibody against Cx43 in transgenic fish with gfp-highlighted endothelial cells. This suggests a potential role of Cx43 in endothelial migration. It is possible that v Cx43 forms gap junction channels with other cell types or functions as hemichannels. To test the function of Cx43 in vascular formation, Cx43 dominant negative mutants (DN) are expressed in an endothelium-specific manner. In order to control the expression of those DNs during the generation of the transgenic zebrafish, a Loxp flanked fluorescent protein expression cassette is inserted between the promoter and DN expression cassette, which will be excised when Cre is introduced. CHAPTER 1. GENERAL LITERATURE REVIEW Most metazoan cells are connected via gap junction channels except blood and skeletal muscle cells (Kumar 1996). Gap junctions are a unique kind of the transmembrane channel in that they span the two layers of the cell membrane and connect the cytoplasm of two cells while being sealed against the extracellular space. Gap junction channels formed by different gap junction proteins that have different permeabilities. The gap junction channels may allow the formation of the polarized distribution of signal molecules over a range of cells connected by gap junctions. This could be important in cell differentiation or physiology (Levin, M., 2007). Connexin genes encode the gap junction proteins and are unique to ...

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“…Furthermore the results with HeLa cells show that the activation of apoptotic reactions is not a non specific effect of ODQ Evidence has accum gulates highly complex cellular functions. It was shown that a reduction of gap junction coupling reduced the differentiation of cultured chick leg bud mesenchymal cells [27], the proliferation and fusion of the myoblast [6,7] and the differentiation of progenitor cells of the retina [28,29]. Additionally, it was observed that inhibition of gap junction coupling was involved in stimulation of apoptosis in granulosa cells [10,20].…”

Section: Discussionmentioning

confidence: 99%

Cell cycle dependent regulation of gap junction coupling and apoptosis in GFSHR-17 granulosa cells

Schlie¹,

Mazur²,

Bintig³

et al. 2010

JBiSE

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Recent results have shown that the level of gap junction coupling could modulate the induction of apoptotic reactions. We previously observed that 1H-[1,2, 4]Oxadiazole[4,3-a]quinoxalin-1-one (ODQ), a blocker of guanylyl cyclase, inhibited gap junction coupling and thereby promoted activation of characteristic apoptotic reactions such as chromatin condensation, DNA strand breaking, and formation of blebs in GFSHR-17 granulosa cells, the in vitro model for granulosa cells of the maturing ovular follicle. In the present report, we focus on the effects of ODQ with respect to the cell cycle in GFSHR-17 granulosa cells. In synchronised GFSHR-17 granulosa cells, the double whole-cell patch-clamp technique revealed that gap junction conductance in mitotic cells was reduced in comparison to cells in interphase. This reduction of gap junction conductance correlated with a reduction of non-phosphorylated Cx43 in mitotic cells. We compared the stimulation of apoptotic reactions by ODQ between cells in mitosis and in interphase. We observed that the induction of both chromatin condensation and DNA strand breaking by ODQ was increased in mitotic cells, as compared to cells in interphase. The effects of ODQ were not observed in HeLa cells that do not express connexins. The results indicate that reduction of gap junction coupling in mitotic GFSHR-17 granulosa cells depends on phosphorrylation of Cx43 and raises the sensitivity to stimulation of apoptosis. We propose that gap junction coupling is involved in regulation of apoptosis of granulosa cells in maturing ovular follicle.

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Multiphoton imaging of chick retinal development in relation to gap junctional communication

Cited by 8 publications

References 22 publications

Interkinetic nuclear migration: beyond a hallmark of neurogenesis

Interkinetic nuclear migration: beyond a hallmark of neurogenesis

A descriptive and functional study of zebrafish Connexin43

Cell cycle dependent regulation of gap junction coupling and apoptosis in GFSHR-17 granulosa cells

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