Is a decrease in cyclic AMP a necessary and sufficient signal for maturation of amphibian oocytes?

Gelerstein, S.; Shapira, Hagit; Dascal, Nathan; Yekuel, Rivkah; Oron, Yoram

doi:10.1016/0012-1606(88)90185-6

Cited by 32 publications

(21 citation statements)

References 34 publications

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“…PKA inhibits the maturation signaling pathway through at least two points: mRNA translation and Cdc25C activation (Duckworth et al, 2002;Matten et al, 1994), consistent with the idea that it is acting as a safety mechanism to eliminate spontaneous maturation in the absence of a positive signal. Although challenging the accepted dogma, our model is supported by earlier studies (Gelerstein et al, 1988;Nader et al, 2014;Noh and Han, 1998;Schmitt and Nebreda, 2002) and the yinyang balance between the mPRβ and cAMP pathways effectively explains the discrepancies in the literature.…”

Section: Discussionsupporting

confidence: 77%

“…Furthermore, some studies found that a decrease in cAMP levels was not sufficient to induce spontaneous maturation, and that an increase in cAMP accelerates maturation (Gelerstein et al, 1988;Noh and Han, 1998). Consistently, exposing oocytes to P4 for <30 min induced a decrease in cAMP but did not induce oocyte maturation, which required ≥30 min incubation with P4 (Nader et al, 2014).…”

Section: Introductionmentioning

confidence: 98%

“…Whereas some studies detect a 10-60% drop in cAMP levels from 15 s up to 6 h after P4 addition (Bravo et al, 1978;Cicirelli and Smith, 1985;Gelerstein et al, 1988;Maller et al, 1979;Mulner et al, 1979;Nader et al, 2014;Sadler and Maller, 1981;SchorderetSlatkine et al, 1982), others failed to detect any changes in cAMP levels in response to P4 (Noh and Han, 1998;O'Connor and Smith, 1976;Schutter et al, 1975;Thibier et al, 1982). Furthermore, some studies found that a decrease in cAMP levels was not sufficient to induce spontaneous maturation, and that an increase in cAMP accelerates maturation (Gelerstein et al, 1988;Noh and Han, 1998).…”

Section: Introductionmentioning

confidence: 99%

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Xenopus oocyte prophase I meiotic arrest is released independently from a decrease in cAMP levels or PKA activity

et al. 2016

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Vertebrate oocytes arrest at prophase of meiosis I as a result of high levels of cyclic adenosine monophosphate (cAMP) and protein kinase A (PKA) activity. In Xenopus, progesterone is believed to release meiotic arrest by inhibiting adenylate cyclase, lowering cAMP levels and repressing PKA. However, the exact timing and extent of the cAMP decrease is unclear, with conflicting reports in the literature. Using various in vivo reporters for cAMP and PKA at the single-cell level in real time, we fail to detect any significant changes in cAMP or PKA in response to progesterone. More interestingly, there was no correlation between the levels of PKA inhibition and the release of meiotic arrest. Furthermore, we devised conditions whereby meiotic arrest could be released in the presence of sustained high levels of cAMP. Consistently, lowering endogenous cAMP levels by >65% for prolonged time periods failed to induce spontaneous maturation. These results argue that the release of oocyte meiotic arrest in Xenopus is independent of a reduction in either cAMP levels or PKA activity, but rather proceeds through a parallel cAMP/PKAindependent pathway.

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Section: Discussionsupporting

confidence: 77%

Section: Introductionmentioning

confidence: 98%

Section: Introductionmentioning

confidence: 99%

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Xenopus oocyte prophase I meiotic arrest is released independently from a decrease in cAMP levels or PKA activity

et al. 2016

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“…They also show that adenosine prevents cAMP reduction in oocytes that are induced to mature with progesterone (26). Despite these discordant results, it has been shown that the cAMP-dependent PKA catalytic subunit inhibits progesterone-induced maturation (38).…”

Section: Resultsmentioning

confidence: 98%

“…It has been suggested that low concentrations of IBMX (30 ,uM) inhibit insulin-induced maturation by arresting cAMPphosphodiesterase activity and, there is a large body of data showing that induction of oocyte maturation results in a decrease of intracellular cAMP (1,35,38,54 (26) showed that acetylcholine treatment of oocytes lowers cAMP levels but does not initiate GVBD (26). They also show that adenosine prevents cAMP reduction in oocytes that are induced to mature with progesterone (26).…”

Section: Resultsmentioning

confidence: 99%

tpr-met oncogene product induces maturation-producing factor activation in Xenopus oocytes.

Daar¹,

White²,

Schuh³

et al. 1991

Mol. Cell. Biol.

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tpr-met, a tyrosine kinase oncogene, is the activated form of the met proto-oncogene that encodes the receptor for hepatocyte growth factor/scatter factor. The tpr-met product (p65tP`-t) was tested for its ability to induce meiotic maturation in Xenopus oocytes. While src and abl tyrosine kinase oncogene products have previously been shown to be inactive in this assay, p65tPr-met efficiently induced maturation-promoting factor (MPF) activation and germinal vesicle breakdown (GVBD) together with the associated increase in ribosomal S6 subunit phosphorylation. tpr-met-mediated MPF activation and GVBD was dependent on the endogenous c_mos,e, while the increase in S6 protein phosphorylation was not significantly affected by the loss of mos function. The phosphodiesterase inhibitor 3-isobutyl-l-methylxanthine inhibits tpr-met-mediated GVBD at concentrations that prevent insulin-but not progesterone-induced oocyte maturation. Moreover, maturation triggered by tpr-met is also inhibited by cyclic AMP-dependent protein kinase. This is the first demonstration that a tyrosine kinase oncogene product, p6V5t-met, can induce meiotic maturation in Xenopus oocytes and activate MPF through a mos-dependent pathway, possibly the insulin or insulinlike growth factor 1 pathway.The c-met proto-oncogene product has recently been identified as the hepatocyte growth factor/scatter factor receptor (7,27). The met proto-oncogene was discovered via the activated oncogene, tpr-met (46), that was generated in a human osteogenic cell line treated with N-methyl-N-nitro-N-nitrosoguanidine (11). Activation resulted from a DNA rearrangement between the tpr sequence from chromosome 1 and downstream met tyrosine kinase receptor sequences located on chromosome 7 (28, 46). The tpr-met product, 5tPr-me6 , induces transformation of NIH 3T3 cells as a constitutively expressed tyrosine kinase (11).The Xenopus oocyte system is useful for examining the events involved in signal transduction (58). Fully grown Xenopus oocytes arrested at the G2/M border (40) can be induced to enter M phase by progesterone, insulin, or insulinlike growth factor 1 (IGF-1). A marked decrease in cyclic AMP (cAMP) levels is an early biochemical change that occurs in oocytes after progesterone treatment. This decrease is due to inhibition of adenylate cyclase (22,31,(49)(50)(51). In contrast, maturation induced by insulin and IGF-1 involves inhibition of adenylate cyclase as well as stimulation of a phosphodiesterase activity (52, 53). The hormones initiate the activation of maturation-promoting factor (MPF), germinal vesicle breakdown (GVBD), chromosome condensation, completion of meiosis I, and progression to metaphase arrest at meiosis II. MPF is a cytoplasmic protein kinase activity that participates in GVBD as well as chromosome condensation (38, 42) and consists of the homologs for the major cell cycle oscillator p34cdc2 and B-type cyclins (15,17,24,25,41,47). The mos proto-oncogene product is required for both progesterone-and insulin-induced oocyte maturation and therefore...

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Inhibition of the adenylyl cyclase and activation of the phosphatidylinositol pathway in oocytes through expression of serotonin receptors does not induce oocyte maturation

Noh

Han

1998

J. Exp. Zool.

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Is a decrease in cyclic AMP a necessary and sufficient signal for maturation of amphibian oocytes?

Cited by 32 publications

References 34 publications

Xenopus oocyte prophase I meiotic arrest is released independently from a decrease in cAMP levels or PKA activity

Xenopus oocyte prophase I meiotic arrest is released independently from a decrease in cAMP levels or PKA activity

tpr-met oncogene product induces maturation-producing factor activation in Xenopus oocytes.

Inhibition of the adenylyl cyclase and activation of the phosphatidylinositol pathway in oocytes through expression of serotonin receptors does not induce oocyte maturation

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