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Mediated Metaphase Arrest in Vertebrate Eggs

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Mediated Metaphase Arrest in Vertebrate Eggs Downloaded from genesdev.cshlp.org on October 1, 2021 - Published by Cold Spring Harbor Laboratory Press REVIEW Under arrest: cytostatic factor (CSF)-mediated metaphase arrest in vertebrate eggs Brian J. Tunquist and James L. Maller1 The Howard Hughes Medical Institute and Department of Pharmacology, University of Colorado School of Medicine, Denver, Colorado 80262, USA In most animals, the development of the immature oo- responsible for the inhibition of mitosis and cleavage. cyte into a fertilizable gamete, a process known as oo- This hypothetical factor from the cytoplasm of maturing cyte maturation, involves an arrest in the meiotic cell oocytes can be tentatively labeled ‘cytostatic factor.’” cycle while awaiting fertilization. Depending on the or- Accordingly, the arrest of vertebrate eggs in meiosis II ganism, this arrest can occur at the beginning of meiosis has since been renamed cytostatic factor (CSF) arrest, I, in metaphase of meiosis I, in metaphase of meiosis II, and the terms mature oocyte, metaphase-arrested oo- or, after the completion of meiosis altogether, in the pro- cyte, meiosis II-arrested oocyte, and CSF-arrested oocyte nuclear stage. In the case of the vertebrate oocyte, matu- are synonymous with the term unfertilized egg. ration begins at the G2/M-phase border of meiosis I, and CSF, by definition, does not describe a single molecule the arrest at the end of oocyte maturation occurs at met- or protein, but rather an activity found in the egg. This aphase of meiosis II. In vertebrates, premature arrest dur- cell division inhibitor must accumulate during oocyte ing oocyte maturation, as well as parthenogenetic re- maturation, must be capable of functioning in meiosis II, lease from the meiosis II arrest, is often the cause of and must be inactivated on fertilization or parthenoge- infertility (Winston et al. 1991; Levran et al. 2002). In netic activation. Since 1971, numerous attempts have addition to gaining insight into the process of infertility, been made to identify CSF(s) in vertebrate eggs and to elucidation of the mechanism of meiotic arrest may in- elucidate the molecular mechanism of the meiotic met- crease our understanding of embryonic development, the aphase arrest. Much of the progress in our understanding molecular signal transduction pathways that operate in of the biochemistry and cell biology of CSF arrest since cell division, and cell cycle controls that may be altered then has come from studies using the denuded oocytes, in cancer cells. embryos, and cell-free extracts of the South African Over 30years ago, Yoshio Masui and Clement Markert clawed frog Xenopus laevis. Although not as extensively (1971) published an historic paper describing cytoplas- studied, the oocytes of higher vertebrates, such as mice, mic control over the behavior of nuclei of both meiotic recapitulate most features of Xenopus oocyte matura- and mitotic cells. This paper described an activity in the tion, and contain components of CSF activity homolo- cytoplasm of eggs from the leopard frog Rana pipiens gous to those that have been identified in the Xenopus that was able to initiate oocyte maturation when in- system (Masui 2000; Kubiak and Ciemerych 2001). To jected into immature G2-arrested oocytes, an activity understand the genesis of CSF activity and the mecha- they termed maturation-promoting factor (MPF). In the nism of its action, it is important to consider the biology same paper, Masui and Markert discovered that micro- and biochemistry of oocyte maturation. injection of the same egg cytoplasm into one blastomere of a two-cell embryo produced a cleavage arrest in the Xenopus oocyte maturation injected blastomere, whereas the uninjected blastomere continued to divide normally. They observed that the Fully grown, immature stage VI oocytes present in the “mitotic apparatus” of the injected blastomere was “ar- ovaries of adult frogs are arrested at the G2/M transition rested at metaphase.” As a control, cytoplasm taken of meiosis I. On progesterone (PG) secretion in vivo by from immature oocytes or early embryos did not inhibit the neighboring follicle cells of the ovary in response to cleavage of the injected blastomere. This led to the sup- pituitary hormones, or on PG addition in culture, the position that a “specific cytoplasmic factor or factors is oocytes enter meiosis I and proceed with the process termed “oocyte maturation,” ultimately resulting in a fertilizable egg (Fig. 1). 1Corresponding author. The biochemistry of oocyte maturation has been rig- E-MAIL [email protected]; FAX (303) 315-7160. Article and publication are at http://www.genesdev.org/cgi/doi/10.1101/ orously studied (for review, see Schmitt and Nebreda gad.1071303. 2002). One reason for this comes from the discovery of GENES & DEVELOPMENT 17:683–710 © 2003 by Cold Spring Harbor Laboratory Press ISSN 0890-9369/03 $5.00; www.genesdev.org 683 Downloaded from genesdev.cshlp.org on October 1, 2021 - Published by Cold Spring Harbor Laboratory Press Tunquist and Maller Figure 1. Pathways involved in oocyte matura- tion. (A) Fully grown immature Xenopus oocytes are arrested at the G2/M border of the meiotic cell cycle. The steroid hormone progesterone overcomes this arrest and causes initiation of oo- cyte maturation. The oocytes enter meiosis I (MI), as witnessed by the appearance of a white spot in the center of the animal hemisphere due to the breakdown of the germinal vesicle (nuclear envelope), ∼3–4 h after progesterone stimulation. This is followed by a transient 50% decline in MPF activity and entry into meiosis II (MII), cul- minating with arrest in metaphase through an activity known as cytostatic factor (CSF). Fertil- ization of the egg overcomes CSF arrest, followed by exit from meiosis II and entry into the embry- onic cell cycles. Two important signal transduc- tion pathways crucial for the process of oocyte maturation are MPF (blue) and p42 MAPK (green; adapted from Ferrell 1999). (B) Pathway of MPF activation. Maturation-promoting factor (MPF) is a heterodimeric complex composed of a Cdc2 protein kinase subunit and a cyclin B regulatory subunit. MPF is found in an inactive form in im- mature oocytes due to phosphorylation on Thr 14 and Tyr 15 on Cdc2 by the dual-specificity inhibitory kinase Myt1. Progesterone stimula- tion of the immature oocyte brings about the ac- tivation of a dual specificity protein phosphatase, Cdc25C, that directly counteracts the Myt1 phosphorylation of MPF, leading to its activa- tion. Progesterone also activates pathways that inhibit the Myt1 kinase. MPF activity is crucial for the process of oocyte maturation by acting pleiotropically to induce chromosome condensa- tion, germinal vesicle breakdown (GVBD), and formation of the meiotic spindle, thus driving en- try into M phase. (C) Activation of the MAPK pathway during oocyte maturation. Progesterone stimulation of the immature oocyte leads to the synthesis of the MAPK kinase kinase (MAPKKK), Mos, from maternal mRNA. Mos activates the MAPK kinase MEK1, which activates MAPK, and MAPK activates the serine/threonine protein kinase p90Rsk. The MAPK pathway facilitates the MPF-driven process of oocyte maturation by contributing to the inhibition of Myt1 during meiosis I. As discussed in the text, this pathway is also crucial for the establishment of CSF arrest in the unfertilized egg in meiosis II. MPF reported in the same article in which Masui and 1989; Gautier and Maller 1991; Mueller et al. 1995a,b). Markert described CSF activity. MPF was regarded as a The steroid hormone PG is now thought to initiate oo- universal regulator of the G2/M transition, and efforts to cyte maturation in nonmammalian vertebrates by bind- characterize it lasted many years. MPF was eventually ing to a recently identified seven-transmembrane G pro- purified in this laboratory and shown to be a heterodimer tein-coupled receptor (GPCR; Zhu et al. 2003a,b), which composed of a catalytic kinase subunit, Cdk1, and a also has close homologs in mammals. PG binding to its regulatory subunit, cyclin B (Dunphy et al. 1988; Gautier GPCR inhibits adenylyl cyclase in a GTP-dependent, et al. 1988, 1990; Lohka et al. 1988). Similar results were pertussis toxin-sensitive manner (Finidori-Lepicard et al. obtained with clam and starfish oocytes (Draetta et al. 1981; Sadler and Maller 1981; Zhu et al. 2003a), and de- 1989; Labbe et al. 1989). Importantly, the Cdk1 subunit creases the level of cAMP within minutes to cause reas- is homologous to the genetically identified yeast cell sociation of the catalytic subunit of cAMP-dependent cycle control gene, cdc2+, which is now regarded as cru- protein kinase (PKA) with the regulatory subunit (Maller cial for the onset of cell division in all cells (Gautier et al. and Krebs 1977; Speaker and Butcher 1977). PKA can 1988; Nurse 1990). inhibit MPF activation even several hours after PG In the immature oocyte, MPF exists as a complex of (Maller and Krebs 1977, 1980; Huchon et al. 1981; Rime Cdc2 (Cdk1) and cyclin B (Cdc2/cyclin B), but is catalyti- et al. 1992; Matten et al. 1994). Recent evidence suggests cally inactive due to inhibitory phosphorylation of threo- the early inhibition by PKA does not require PKA kinase nine 14 (Thr 14) and tyrosine 15 (Tyr 15) residues by the activity, whereas the late inhibition does (Duckworth et dual-specificity kinase Myt1 (Fig. 1B; Gautier et al. al. 2002; Schmitt and Nebreda 2002). The PG-mediated 684 GENES & DEVELOPMENT Downloaded from genesdev.cshlp.org on October 1, 2021 - Published by Cold Spring Harbor Laboratory Press CSF arrest in vertebrate eggs decrease in the level of cAMP is followed by an increase within 30min after PG binding (Sagata et al. 1988; in protein synthesis, and a few hours later germinal Sheets et al. 1994, 1995). The up-regulation of mos trans- vesicle (nuclear) breakdown (GVBD) occurs, as evidenced lation is a result of complex changes that occur at the morphologically by the appearance of a white spot in the 3Ј-UTR of mos mRNA, which enable its cytoplasmic center of the pigmented animal pole (Fig.
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