Role of Mitogen Activated Protein Kinase and Maturation Promoting Factor During the Achievement of Meiotic Competency in Mammalian Oocytes

Abstract

The oocyte quality remains as one of the major problems associated with poor in vitro fertilization (IVF) rate and assisted reproductive technology (ART) failure worldwide. The oocyte quality is dependent on its meiotic maturation that begins inside the follicular microenvironment and gets completed at the time of ovulation in most of the mammalian species. Follicular oocytes are arrested at diplotene stage of first meiotic prophase. The resumption of meiosis from diplotene arrest, progression through metaphase-I (M-I) and further arrest at metaphase-II (M-II) are important physiological requirements for the achievement of meiotic competency in mammalian oocytes. The achievement of meiotic competency is dependent upon cyclic stabilization/destabilization of maturation promoting factor (MPF). The mitogen-activated protein kinase3/1 (MAPK3/1) modulates stabilization/destabilization of MPF in oocyte by interacting either with signal molecules, transcription and post-transcription factors in cumulus cells or cytostatic factors (CSFs) in oocyte. MPF regulates meiotic cell cycle progression from diplotene arrest to M-II arrest and directly impacts oocyte quality. The MAPK3/1 activity is not reported during spontaneous meiotic resumption but its activity in cumulus cells is required for gonadotropin-induced oocyte meiotic resumption. Although high MAPK3/1 activity is required for the maintenance of M-II arrest in several mammalian species, its cross-talk with MPF remains to be elucidated. Further studies are required to find out the MAPK3/1 activity and its impact on MPF destabilization/stabilization during achievement of meiotic competency, an important period that decides oocyte quality and directly impacts ARTs outcome in several mammalian species including human. J. Cell. Biochem. 119: 123-129, 2018. © 2017 Wiley Periodicals, Inc.

Inability to Maintain Metaphase-II Arrest due to Increase of Reactive Oxygen Species in Rat Eggs

“…Similarly, increase of Thr-14/Tyr-15 and decrease of Thr-161 phosphorylated Cdk1 level resulted in EM-II and thereby abortive SEA in rat [5][6][7] and mouse eggs [37,38] cultured in vitro. The modulation of Cdk1 specific phosphorylation status could induce cyclin B1 dissociation and degradation [33][34][35][36][37][38]. Our results suggested that cyclin B1 level decreased significantly during EM-II ( Figure 2D2) as compared to control eggs ( Figure 2D1) and further supported by CTCF analysis (Figure 2D3; p < 0.001).…”

“…i.e., cyclin-dependent kinase 1 (Cdk1) and a regulatory subunit, i.e., cyclin B1 [6,7,33,34]. However, changes in Cdk1 activity as well as MPF destabilization may also occur due to increase of mitogen-activated protein kinase (MAPK) [35]. This statement is supported by the observations that MAPK modulates Cdk1 activity and destabilizes MPF during spontaneous exit from M-II arrest [22,23].…”

Journey of oocyte from metaphase‐I to metaphase‐II stage in mammals

“…Studies suggest that several enzymes, factors and signal molecules are involved during cell cycle progression from M‐I to M‐II stage and formation as well as extrusion of PB‐I that enable an oocyte to get converted into a good quality ovum (Miao, Kikuchi, Sun, & Schatten, ). The quality of ovum directly impacts the reproductive as well as ART outcome (Prasad, Tiwariet al, ; Tiwari et al, ; Tiwari, Tripathi, & Chaube, ). This review article focuses and updates the information on molecular and cellular changes during journey of oocyte from M‐I to M‐II stage and extrusion of PB‐I in mammalian oocytes (Figure).…”

“…Molecular interactions through several pathways result in sub cellular as well as cellular changes during meiotic cell cycle progression from M‐I to M‐II stage in mammalian species. The cytostatic factors (CSFs) regulate maturation promoting factor (MPF) activity and modulate oocyte meiosis in rats (Tiwari & Chaube, ; Tiwari et al, ). MPF activity is high at M‐I stage and drops during meiotic exit from M‐I but increases at M‐II arrest in mouse oocytes (Terret et al, ).…”

“…The functional SAC proteins exist in mouse oocytes arrested at M‐I stage (Li et al, ; Wassmann, Niault, & Maro, ). Mad2 is one of the major SAC proteins that play an important role during meiotic cell cycle progression and extrusion of PB‐I in oocyte (Tiwari et al, ; Tripathi et al, ). Mad2 regulate cytokinesis by controlling the activity of mitotic kinesin like protein 2 (MKlp2) (Kitagawa, Fung, Onishi, Saya, & Lee, : Lee, McCormick, & Saya, ).…”