Germinal vesicle migration and dissolution in Rana pipiens oocytes: effect of steroids and microtubule poisons

Lessman, Charles A.

doi:10.1016/0045-6039(87)90469-6

Cited by 30 publications

(21 citation statements)

References 28 publications

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“…Therefore, it is likely that other factors, in addition to Ca 2+ release, are required for GVBD. The fact that nocodazole and Colcemid enhance the effects of progesterone on the induction of GVBD whilst taxol diminishes it (Skoblina and Kondratieva 1982;Lessman et al 1986;Lessman 1987), that taxol can inhibit InsP 3 -induced Ca 2+ release from microsomes (Duesbery and Masui 1996) and that β-tubulin dissociates from the ER during maturation (Duesbery and Masui 1993) suggests the involvement of microtubule depolymerization in oocyte maturation. Therefore, it is possible that microtubule depolymerization is required in conjunction with Ca 2+ release during progesterone-induced GVBD.…”

Section: Discussionmentioning

confidence: 96%

“…Early workers have observed that colchicine enhances pituitary-induced ovulation in frogs, in vivo as well as in vitro (McPhail and Wilbur 1943;Wright 1962). More recently, it was observed that inducing microtubule depolymerization with nocodazole or Colcemid could enhance the effect of progesterone on the oocyte while preventing microtubule depolymerization with taxol could diminish it (Skoblina and Kondratieva 1982;Lessman et al 1986;Lessman 1987). These observations led us to examine the hypothesis that microtubule depolymerization is required in conjunction with intracellular Ca 2+ release during oocyte maturation.…”

Section: Kinetic Analysis Of 45 Ca 2+ Mobilizationmentioning

confidence: 94%

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The role of Ca 2+ in progesterone-induced germinal vesicle breakdown of Xenopus laevis oocytes: the synergic effects of microtubule depolymerization and Ca 2+

Duesbery

Masui

1996

Development Genes and Evolution

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By monitoring (45)Ca(2+) influx and efflux from oocytes a transient increase followed by a transient decrease in the Ca(2+)-content of progesterone-treated oocytes was observed. Chelation of intracellular Ca(2+) with EGTA or BAPTA-type buffers inhibited progesterone-induced GVBD. Buffers with a mid-range Kd (∼1.5 μM) were most effective in inhibiting GVBD whereas buffers with a Kd above or below this value were less effective. These observations indicate that intracellular Ca(2+), probably in the form of a localized release, is required for progesterone-induced oocyte maturation. However, Ca(2+) alone was insufficient to induce GVBD. When the effects of nocodazole and taxol upon this Ca(2+)-requirement were tested, we observed that taxol-induced microtubule polymerization not only delayed progesterone-induced GVBD but also completely inhibited it in combination with BAPTA-AM. Conversely, nocodazole-induced microtubule depolymerization in combination with ionophore A23187 not only accelerated progesterone-induced GVBD, but also induced GVBD in the absence of progesterone. The combined treatment of oocytes with nocodazole and InsP3, or with cold treatment and ionophore A23187 also induced GVBD in the absence of progesterone. Thus, Ca(2+) and microtubule depolymerization synergistically promote GVBD. In both nocodazole- and cold-treated oocytes, the GV was displaced to the periphery of the oocyte and underwent GVBD when treated with A23187. However, when the GV was displaced to the cortex by a centrifugal force under conditions that would not cause microtubule depolymerization and the oocyte was treated with A23187, oocytes did not undergo GVBD.

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Section: Discussionmentioning

confidence: 96%

Section: Kinetic Analysis Of 45 Ca 2+ Mobilizationmentioning

confidence: 94%

The role of Ca 2+ in progesterone-induced germinal vesicle breakdown of Xenopus laevis oocytes: the synergic effects of microtubule depolymerization and Ca 2+

Duesbery

Masui

1996

Development Genes and Evolution

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“…This strongly suggests that the interactions between microtubules and microfilaments play an important role in the formation and persistence of the demecolcine-induced cytoplasmic protrusions. Studies showed that demecolcine enhanced centrifugation-induced germinal vesicle migration in Rana pipiens oocytes by lowering the ooplasmic viscoelasticity (Lessman, 1987). Studies also showed that spindle microtubules were involved in organizing the contractile apparatus of dividing cultured cells (Fishkind et al, 1996).…”

Section: Demecolcine-assisted Enucleation Of Goat Oocytes 197mentioning

confidence: 96%

Demecolcine-Assisted Enucleation of Goat Oocytes: Protocol Optimization, Mechanism Investigation, and Application to Improve the Developmental Potential of Cloned Embryos

Lan

Han

et al. 2008

Cloning and Stem Cells

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Although demecolcine-assisted enucleation has been performed successfully in porcine and cattle, the mechanism and protocol optimization of chemically assisted enucleation need further investigation. The present study optimized the protocol for goat oocyte enucleation and demonstrated that a 30-min treatment with 0.8 ng/mL demecolcine-induced cytoplasmic protrusions in over 90% of the oocytes. Rates of enucleation, cell fusion, and blastocyst formation were significantly higher after demecolcine-assisted than after blind aspiration enucleation, although differences in rates of live births remain to be unequivocally determined between the two treatments. The ability to form protrusions decreased significantly as spindles became less organized in aged oocytes and the oocytes with a poor cumulus expansion. More than 93% of the demecolcine-induced protrusions persisted for 2 h in the absence of cytochalasin B (CB) but most disappeared within 30 min of CB treatment. The spindle disintegrated, an actin-rich ring formed around the chromosome mass and the MAP kinase activity increased significantly after demecolcine treatment. When oocytes with induced protrusions were treated with CB, however, the contractile ring disappeared, the spindle reintegrated, and both MPF and MAP kinase activities decreased significantly. It is concluded that (1) cytoplasmic protrusions can be induced in goat oocytes with a very low concentration of demecolcine; (2) oocyte selection and enucleation can be achieved simultaneously with demecolcine treatment; and (3) an interactive effect between the MAP kinase, MPF, microfilaments and microtubules might be implicated in the control of cytoplasmic protrusion formation after demecolcine treatment.

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“…While the role of MTs and associated motor proteins in non-mammalian oocyte and early embryonic development is well documented (Elinson and Rowning, 1988; Gard, 1991; Lane and Allan, 1999; Lessman, 1987; Schroeder and Gard, 1992; Yisraeli et al, 1990), less is known about the MT network during early mammalian development. However, several mouse studies have shown that MT are required for formation of MT organizing centers and the meiotic spindle apparatus, polar body extrusion, pronuclear migration, and mitotic spindle formation in early embryos (Calarco-Gillam et al, 1983; Maro et al, 1990; Maro and Verlhac, 2002; Schatten et al, 1985) More recently, oocyte MTs have also been found to drive endoplasmic reticulum (ER) and mitochondrial re-targeting during oocyte maturation (FitzHarris et al, 2007; Mehlmann et al, 1995; Van Blerkom, 1991; Van Blerkom and Runner, 1984).…”

Section: Introductionmentioning

confidence: 99%

Regulation of mouse oocyte microtubule and organelle dynamics by PADI6 and the cytoplasmic lattices

Kan

Yurttas

Kim

et al. 2011

Developmental Biology

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Organelle positioning and movement in oocytes is largely mediated by microtubules (MTs) and their associated motor proteins. While yet to be studied in germ cells, cargo trafficking in somatic cells is also facilitated by specific recognition of acetylated MTs by motor proteins. We have previously shown that oocyte-restricted PADI6 is essential for formation of a novel oocyte-restricted fibrous structure, the cytoplasmic lattices (CPLs). Here, we show that α-tubulin appears to be associated with the PADI6/CPL complex. Next, we demonstrate that organelle positioning and redistribution is defective in PADI6-null oocytes and that alteration of MT polymerization or MT motor activity does not induce organelle redistribution in these oocytes. Finally, we report that levels of acetylated microtubules are dramatically suppressed in the cytoplasm of PADI6-null oocytes, suggesting that the observed organelle redistribution failure is due to defects in stable cytoplasmic MTs. These results demonstrate that the PADI6/CPL superstructure plays a key role in regulating MT-mediated organelle positioning and movement.

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Germinal vesicle migration and dissolution in Rana pipiens oocytes: effect of steroids and microtubule poisons

Cited by 30 publications

References 28 publications

The role of Ca 2+ in progesterone-induced germinal vesicle breakdown of Xenopus laevis oocytes: the synergic effects of microtubule depolymerization and Ca 2+

The role of Ca 2+ in progesterone-induced germinal vesicle breakdown of Xenopus laevis oocytes: the synergic effects of microtubule depolymerization and Ca 2+

Demecolcine-Assisted Enucleation of Goat Oocytes: Protocol Optimization, Mechanism Investigation, and Application to Improve the Developmental Potential of Cloned Embryos

Regulation of mouse oocyte microtubule and organelle dynamics by PADI6 and the cytoplasmic lattices

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