Oocyte meiotic maturation includes large-scale chromatin remodeling as well as cytoskeleton and nuclear envelope rearrangements. This review addresses the dynamics of key cytoskeletal proteins (tubulin, actin, vimentin, and cytokeratins) and nuclear envelope proteins (lamin A/C, lamin B, and the nucleoporin Nup160) in parallel with chromatin reorganization in maturing mouse oocytes. A major feature of this reorganization is the concentration of heterochromatin into a spherical perinucleolar rim called surrounded nucleolus or karyosphere. In early germinal vesicle (GV) oocytes with non-surrounded nucleolus (without karyosphere), lamins and Nup160 are at the nuclear envelope while cytoplasmic cytoskeletal proteins are outside the nucleus. At the beginning of karyosphere formation, lamins and Nup160 follow the heterochromatin relocation assembling a new spherical structure in the GV. In late GV oocytes with surrounded nucleolus (fully formed karyosphere), the nuclear envelope gradually loses its integrity and cytoplasmic cytoskeletal proteins enter the nucleus. At germinal vesicle breakdown, lamin B occupies the karyosphere interior while all the other proteins stay at the karyosphere border or connect to chromatin. In metaphase oocytes, lamin A/C surrounds the spindle, Nup160 localizes to its poles, actin and lamin B are attached to the spindle fibers, and cytoplasmic intermediate filaments associate with both the spindle fibers and the metaphase chromosomes.

Observations of the processes of oogenesis, fertilization, and the earliest embryonic development have given us the opportunity to estimate the importance of chromosomal distribution errors for the success of mammalian reproduction. It is now known that in the large volume of oocytes, zygotes and the first embryonic cells, the rearrangement of chromatin is associated with a complex rearrangement of cytoskeletal structures, which creates specific problems. This review discusses two main issues critical to the success of early embryos: Why oocyte meiosis is too frequently wrong in chromosomal segregation? Why the first zygotic mitoses are too frequently wrong in chromosomal segregation? We concluded the following: (1) The main cytoskeletal defects that disturb oocyte meiosis are a problematic connection between cytoskeleton and nucleoskeleton, unsuccessful movement of the spindle to the oocyte periphery, unstable anchoring of the spindle to oolemma, and deviations in meiotic spindle morphology; (2) The main cytoskeletal defects that disturb pronuclear unification are nonfunctional male centriole, unsuccessful forming of microtubule aster around the sperm centrosome, problematic movement of the two pronuclei towards each other and inappropriate contacts between centrosomes, microtubules and nuclear pore complexes; (3) Cytoskeletal defects that disturb zygote mitosis are unsuccessful forming of bipolar mitotic spindle, non-synchronized congression of maternal and paternal chromosomes, and unsuccessful attachment of kinetochores to microtubules.

Systemic lupus erythematosus is an autoimmune disease that mainly affects women of reproductive age. Its pathological manifestations directly and indirectly negatively affect the ovarian reserve, the quality of oocytes, and the precise mechanisms of meiosis. This review presents the molecular mechanisms by which lupus damages ovarian tissue and meiosis in oocytes. The role of chronic inflammation, impaired hormonal levels, and the presence of specific autoantibodies are considered. The available data on how oocyte structures (meiotic spindle, actin cytoskeleton, membrane organelles and chromatin) are damaged by lupus symptoms are summarized.

Background/Objectives: Osteoarthritis has been increasingly described as associated with systemic inflammation, raising the question of how it would affect fertility in young women with or without reproductive hormone administration. We studied oogenesis in mice with collagenase-induced osteoarthritis (CIOA) as a model system with fewer ethical limitations after estradiol (E2) or follicle-stimulating hormone (FSH) treatment. Methods: Oocytes have been isolated from mice subjected to various treatment regimens. The meiotic spindle, the chromatin, and the actin cap were fluorescently labeled and analyzed. Results: In addition to reduced maturation rates, specific oocyte abnormalities were registered when CIOA, FSH, or E2 were applied in isolation. Combined treatments showed that the spindle, chromatin, and actin cytoskeleton parameters were differently affected in oocytes from groups with CIOA treated by estradiol and those treated with FSH. Enlarged spindles, ooplasmic tubulin asters, aligned metaphases, and predominantly normal actin caps, often with an actin halo, were typical for groups with CIOA combined with estradiol. The groups with CIOA and FSH had slightly enlarged spindles, unaligned metaphases with degenerated chromatin surrounded by a cloud of depolymerized tubulin, and small actin caps. Conclusions: Our results show that experimental osteoarthritis with or without exogenous reproductive hormones negatively affects oogenesis, presumably due to systemic inflammatory factors making the ovarian microenvironment less capable of supporting oocyte maturation. Estradiol supplementation does not benefit oogenesis. FSH treatment induced cytoskeletal and chromatin abnormalities that presumably disturb the fertilization and development potential of affected oocytes. These data can have implications for assisted reproduction in cases of patients with osteoarthritis.