2006
DOI: 10.1111/j.1440-169x.2006.00895.x
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Activator of G‐protein signaling in asymmetric cell divisions of the sea urchin embryo

Abstract: An asymmetric fourth cell division in the sea urchin embryo results in formation of daughter cells, macromeres and micromeres, with distinct sizes and fates. Several lines of functional evidence presented here, including pharmacological interference and dominant negative protein expression, indicate that heterotrimeric G protein Gi and its interaction partner, activator of G-protein signaling (AGS), are necessary for this asymmetric cell division. Inhibition of Gi signaling by pertussis toxin interferes with m… Show more

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Cited by 19 publications
(17 citation statements)
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References 31 publications
(90 reference statements)
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“…However, an intrinsic timing mechanism appears to exist since the vegetal cortex loses pigment granules during micromere formation at the 8 to 16-cell stage, even in cleavage arrested fertilized eggs (Schroeder, 1980). Concerning the molecular mechanism controlling UCD in sea urchin, an orthologue of the LGN/Pins protein was found to be involved (Voronina and Wessel, 2006). How the vegetal cortical enrichment of Pins/LGN is triggered at the 8-cell stage to cause UCD is not known, although it is tempting to speculate that it has something to do with the intrinsic timing mechanism that induces the loss of pigment granules from the vegetal cortex.…”
Section: Ucd In Sea Urchin (Cortical Pulling?)mentioning
confidence: 99%
“…However, an intrinsic timing mechanism appears to exist since the vegetal cortex loses pigment granules during micromere formation at the 8 to 16-cell stage, even in cleavage arrested fertilized eggs (Schroeder, 1980). Concerning the molecular mechanism controlling UCD in sea urchin, an orthologue of the LGN/Pins protein was found to be involved (Voronina and Wessel, 2006). How the vegetal cortical enrichment of Pins/LGN is triggered at the 8-cell stage to cause UCD is not known, although it is tempting to speculate that it has something to do with the intrinsic timing mechanism that induces the loss of pigment granules from the vegetal cortex.…”
Section: Ucd In Sea Urchin (Cortical Pulling?)mentioning
confidence: 99%
“…2012) which have rarely been combined with biochemical studies. This ambiguity applies to the potential role of protein kinases in regulation of ion channel permeability in the oocyte plasma membrane, heterotrimeric G protein activation in sea urchin oocytes (Voronina & Wessel 2006), as well as the fertilization-induced changes in Protein Tyrosine Kinase (PTK) signaling that occur in many marine invertebrate, fish, and amphibian oocytes(Giusti et al . 1999; Tokmakov et al .…”
Section: Introductionmentioning
confidence: 99%
“…This evidence includes pharmacological interference and dominant‐negative protein expression, both indicating that the heterotrimeric G protein Gi and its interaction partner, activator of G‐protein signaling (AGS), are necessary for the asymmetric cell divisions in many organisms such as Drosophila , C. elegans , and mammals (Morin and Bellaïche, ). The AGS/Pins (activator of G‐protein signaling/partner of inscuteable) family of proteins are conserved, multi‐domain molecular scaffolds found in many organisms from yeast to humans, and are reported to be involved in asymmetric cell divisions so far in Drosophila , C. elegans , and sea urchins (Schaefer et al, ; Betschinger and Knoblich, ; Voronina and Wessel, ; Park and Rose, ; Krueger et al, ; Morin and Bellaïche, ). In the sea urchin, inhibition of Gαi signaling by pertussis toxin interfered with micromere formation and led to defects in embryogenesis (Voronina and Wessel, ).…”
Section: Introductionmentioning
confidence: 99%