The caenorhabditis elegans innexin INX-3 is localized to gap junctions and is essential for embryonic development

Starich, Todd A; Miller, A.; Nguyen, Rachel; Hall, David H.; Shaw, Joseph W.

doi:10.1016/s0012-1606(02)00116-1

Cited by 50 publications

(54 citation statements)

References 66 publications

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“…However, expressions appeared in the primary oocytes and fertilized eggs on the surface of infusorigens, suggesting this innexin mRNA was maternal, for use in early embryonic stages. In C. elegans embryos, the zygotic innexin was expressed after the 28-cell stage (Starich et al, 2003). In dicyemids, innexin appears again after the 24-cell stage, suggesting the zygotic expression.…”

Section: Discussionmentioning

confidence: 97%

“…Several, organ-specific innexin genes were reported in a leech, H. medicinalis (Dykes and Macagno, 2006), in Drosophila melanogaster (Drosophilidae) (Stebbings et al, 2002), and in C. elegans (Starich et al, 2003;Chuang et al, 2007;Whitten and Miller, 2007). In embryonic stages, they were exclusively expressed in germ layers, but the dicyemid innexin was expressed in all blastomeres of developing embryos after the 24-cell stage.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

The Expression of Tubulin and Tektin Genes in Dicyemid Mesozoans (Phylum: Dicyemida)

Ogino

Tsuneki

Furuya

2007

Journal of Parasitology

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Section: Discussionmentioning

confidence: 97%

Section: Discussionmentioning

confidence: 99%

The Expression of Tubulin and Tektin Genes in Dicyemid Mesozoans (Phylum: Dicyemida)

Ogino

Tsuneki

Furuya

2007

Journal of Parasitology

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“…Alternatively, PAPS may pass through the gap junctions that permit the exchange of molecules, such as cAMP, between attached cells. Interestingly, a mutant worm of the inx-3 gene encoding a gap junction protein shows an epidermal elongation defect (51).…”

Section: Discussionmentioning

confidence: 99%

Essential Roles of 3′-Phosphoadenosine 5′-Phoshosulfate Synthase in Embryonic and Larval Development of the Nematode Caenorhabditis elegans

Dejima

Seko

Yamashita

et al. 2006

Journal of Biological Chemistry

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Sulfation of biomolecules, which is widely observed from bacteria to humans, plays critical roles in many biological processes. All sulfation reactions in all organisms require activated sulfate, 3-phosphoadenosine 5-phosphosulfate (PAPS), as a universal donor. In animals, PAPS is synthesized from ATP and inorganic sulfate by the bifunctional enzyme, PAPS synthase. In mammals, genetic defects in PAPS synthase 2, one of two PAPS synthase isozymes, cause dwarfism disorder, but little is known about the consequences of the complete loss of PAPS synthesis. To define the developmental role of sulfation, we cloned a Caenorhabditis elegans PAPS synthasehomologous gene, pps-1, and depleted expression of its product by isolating the deletion mutant and by RNA-mediated interference. PPS-1 protein exhibits specific activity to form PAPS in vitro, and disruption of the pps-1 gene by RNAi causes pleiotropic developmental defects in muscle patterning and epithelial cell shape changes with a decrease in glycosaminoglycan sulfation. Additionally, the pps-1 null mutant exhibits larval lethality. These data suggest that sulfation is essential for normal growth and integrity of epidermis in C. elegans. Furthermore, reporter analysis showed that pps-1 is expressed in the epidermis and several gland cells but not in neurons and muscles, indicating that PAPS in the neurons and muscles is provided by other cells.Body and tissue morphologies are generated by orchestrated events of cell movements and cell shape changes at an appropriate time and place. In the nematode Caenorhabditis elegans, which is an ideal model organism for the study of morphogenesis, embryos undergo a 4-fold increase in length and a 3-fold decrease in circumference without cell division after the cell proliferation phase (1). The elongation process requires proper patterning and shape change of the epidermis (hypoderms) and body wall muscle cells adjacent to the hypodermis in C. elegans (2, 3). In the patterning and shape change of the hypodermis and the body wall muscle, both the basement membrane, which is positioned between them, and dynamic cytoskeletal changes play an important role (2, 3). On the other hand, the extracellular cuticle that surrounds the hypodermis contributes to the maintenance of the final shape of the worms after the elongation (1).Sulfation, a common chemical modification of biomolecules, is critical for many biological processes. For example, sulfation of lipooligosaccharide signals determines the symbiosis between the bacteria Rhizobium meliloti and alfalfa (4). In vertebrates, tyrosine sulfation of chemokine receptor CCR5 facilitates HIV entry (5), and terminal SO 4 -4GalNAc of the pituitary hormone lutropin, which plays a critical role in the expression of hormone activity, modulates the circulatory half-life of the hormone (6). Proper sulfation of glycosaminoglycans (GAGs) 2 is required for interactions with several extracellular signaling molecules; therefore, disrupting the genes that encode enzymes mediating sulfation reactions caus...

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“…GJC is increasingly recognized as being involved in regulation of patterning signals in vertebrate and invertebrate pattern formation (Bauer et al, 2001(Bauer et al, , 2002Starich et al, 2003;Nogi and Levin, 2005;Lehmann et al, 2006). Such morphogenetic control could be exerted by GJC-mediated changes in differentiation (Zhang et al, 2002;Araya et al, 2003Araya et al, , 2005Gu et al, 2003;Hirschi et al, 2003), proliferation (Paraguassu-Braga et al, 2003;Pearson et al, 2005), or cell migration (Minkoff et al, 1997;Huang et al, 1998;Lecanda et al, 2000;OviedoOrta et al, 2002;Kjaer et al, 2004).…”

Section: Behavior Is Dependent Upon Gap Junction (Gj) -Mediated Signalsmentioning

confidence: 99%

Mathematical model of morphogen electrophoresis through gap junctions

Esser

Smith

Weaver

et al. 2006

Developmental Dynamics

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Gap junctional communication is important for embryonic morphogenesis. However, the factors regulating the spatial properties of small molecule signal flows through gap junctions remain poorly understood. Recent data on gap junctions, ion transporters, and serotonin during left-right patterning suggest a specific model: the net unidirectional transfer of small molecules through long-range gap junctional paths driven by an electrophoretic mechanism. However, this concept has only been discussed qualitatively, and it is not known whether such a mechanism can actually establish a gradient within physiological constraints. We review the existing functional data and develop a mathematical model of the flow of serotonin through the early Xenopus embryo under an electrophoretic force generated by ion pumps. Through computer simulation of this process using realistic parameters, we explored quantitatively the dynamics of morphogen movement through gap junctions, confirming the plausibility of the proposed electrophoretic mechanism, which generates a considerable gradient in the available time frame. The model made several testable predictions and revealed properties of robustness, cellular gradients of serotonin, and the dependence of the gradient on several developmental constants. This work quantitatively supports the plausibility of electrophoretic control of morphogen movement through gap junctions during early left-right patterning. This conceptual framework for modeling gap junctional signaling-an epigenetic patterning mechanism of wide relevance in biological regulation-suggests numerous experimental approaches in other patterning systems.

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The caenorhabditis elegans innexin INX-3 is localized to gap junctions and is essential for embryonic development

Cited by 50 publications

References 66 publications

The Expression of Tubulin and Tektin Genes in Dicyemid Mesozoans (Phylum: Dicyemida)

The Expression of Tubulin and Tektin Genes in Dicyemid Mesozoans (Phylum: Dicyemida)

Essential Roles of 3′-Phosphoadenosine 5′-Phoshosulfate Synthase in Embryonic and Larval Development of the Nematode Caenorhabditis elegans

Mathematical model of morphogen electrophoresis through gap junctions

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