During meiosis, the homologous chromosomes pair and recombine, a process essential for generating genetically
distinct haploid cells. The unique behavior displayed by meiotic chromosomes has been linked to the activities of a
meiosis-specific supramolecular proteinaceous structure, the synaptonemal complex (SC). Three meiosis-specific
components of the SC have been characterized in mammals, SC protein-1 (SYCP1), -2 (SYCP2), and
-3 (SYCP3).
NCBI Summary:
This gene encodes an essential structural component of the synaptonemal complex. This complex is involved in synapsis, recombination and segregation of meiotic chromosomes. Mutations in this gene are associated with azoospermia in males and susceptibility to pregnancy loss in females. Alternate splicing results in multiple transcript variants that encode the same protein. [provided by RefSeq, May 2010]
DiCarlo A, et al 2000 reported that the meiotic specific synaptonemal complex protein SCP3 is
expressed by female and male primordial germ cells of the mouse
embryo
The synaptonemal complex proteins SCP3 and SCP1 are components of the
synaptonemal complex, a meiosis-specific protein structure essential for
synapsis of homologous chromosomes.
Using polyclonal antibodies raised against
SCPs of rat testis, the expression of these proteins in
embryonic germ cells of the mouse embryo was studied using immunohistochemistry and
immunoblotting. The results support the hypothesis that primordial germ cells are
programmed to enter meiosis unrespective of the sex and that foetal testis
produces a factor that inhibits such programme.
Expression regulated by
Steroids
Comment
Molecular analysis of the effects of steroid hormones on mouse meiotic prophase I progression. Burks DM et al. (2019) Infertility is linked to depletion of the primordial follicle pool consisting of individual oocytes arrested at the diplotene stage of meiotic prophase I surrounded by granulosa cells. Primordial germ cells, the oocyte precursors, begin to differentiate during embryonic development. These cells migrate to the genital ridge and begin mitotic divisions, remaining connected, through incomplete cytokinesis, in clusters of synchronously dividing oogonia known as germ cell cysts. Subsequently, they enter meiosis, become oocytes and progress through prophase I to the diplotene stage. The cysts break apart, allowing individual oocytes to be surrounded by a layer of granulosa cells, forming primordial follicles each containing a diplotene arrested oocyte. A large number of oocytes are lost coincident with cyst breakdown, and may be important for quality control of primordial follicle formation. Exposure of developing ovaries to exogenous hormones can disrupt cyst breakdown and follicle formation, but it is unclear if hormones affect progression of oocytes through prophase I of meiosis. Fetal ovaries were treated in organ culture with estradiol, progesterone, or both hormones, labeled for MSY2 or Synaptonemal complex protein 3 (SYCP3) using whole mount immunocytochemistry and examined by confocal microscopy. Meiotic prophase I progression was also followed using the meiotic surface spread technique. MSY2 expression in oocytes was reduced by progesterone but not estradiol or the hormone combination. However, while MSY2 expression was upregulated during development it was not a precise marker for the diplotene stage. We also followed meiotic prophase I progression using antibodies against SYCP3 using two different methods, and found that the percent of oocytes at the pachytene stage peaked at postnatal day 1. Finally, estradiol and progesterone treatment together but not either alone in organ culture increased the percent of oocytes at the pachytene stage. We set out to examine the effects of hormones on prophase I progression and found that while MSY2 expression was reduced by progesterone, MSY2 was not a precise diplotene stage marker. Using antibodies against SYCP3 to identify pachytene stage oocytes we found that progesterone and estradiol together delayed progression of oocytes through prophase I.//////////////////
Ovarian localization
Primordial Germ Cell, Oocyte
Comment
Germline stem cells and follicular renewal in the postnatal mammalian ovary
Johnson J, et al .
A basic doctrine of reproductive biology is that most mammalian females lose the capacity for germ-cell renewal during fetal life, such that a fixed reserve of germ cells (oocytes) enclosed within follicles is endowed at birth. Here we show that juvenile and adult mouse ovaries possess mitotically active germ cells that, based on rates of oocyte degeneration (atresia) and clearance, are needed to continuously replenish the follicle pool. Consistent with this, treatment of prepubertal female mice with the mitotic germ-cell toxicant busulphan eliminates the primordial follicle reserve by early adulthood without inducing atresia. Furthermore, we demonstrate cells expressing the meiotic entry marker synaptonemal complex protein 3 in juvenile and adult mouse ovaries. Wild-type ovaries grafted into transgenic female mice with ubiquitous expression of green fluorescent protein (GFP) become infiltrated with GFP-positive germ cells that form follicles. Collectively, these data establish the existence of proliferative germ cells that sustain oocyte and follicle production in the postnatal mammalian ovary.
Follicle stages
Comment
Phenotypes
Mutations
2 mutations
Species: mouse
Mutation name: None
type: null mutation fertility: subfertile Comment: Genetic Evidence that Synaptonemal Complex Axial Elements Govern Recombination Pathway Choice in Mice. Li XC et al. Chiasmata resulting from interhomolog recombination are critical for proper chromosome segregation at meiotic metaphase I, thus preventing aneuploidy and consequent deleterious effects. Recombination in meiosis is driven by programmed induction of double strand breaks (DSBs), and the repair of these breaks occurs primarily by recombination between homologous chromosomes, not sister chromatids. Almost nothing is known about the basis for recombination partner choice in mammals. We addressed this problem using a genetic approach. Since meiotic recombination is coupled with synaptonemal complex (SC) morphogenesis, we explored the role of axial elements - precursors to the lateral element in the mature SC - in recombination partner choice, DSB repair pathways, and checkpoint control. Female mice lacking the SC axial element protein SYCP3 produce viable, but often aneuploid, oocytes. We describe genetic studies indicating that while DSB-containing Sycp3(-/-) oocytes can be eliminated efficiently, those that survive have completed repair before the execution of an intact DNA damage checkpoint. We find that the requirement for DMC1 and TRIP13, proteins normally essential for recombination repair of meiotic DSBs, is substantially bypassed in Sycp3 and Sycp2 mutants. This bypass requires RAD54, a functionally conserved protein that promotes intersister recombination in yeast meiosis and mammalian mitotic cells. Immunocytological and genetic studies indicated that the bypass in Sycp3(-/-) Dmc1(-/-) oocytes was linked to increased DSB repair. These experiments lead us to hypothesize that axial elements mediate the activities of recombination proteins to favor interhomolog, rather than intersister recombinational repair of genetically programmed DSBs in mice. The elimination of this activity in SYCP3- or SYCP2-deficient oocytes may underlie the aneuploidy in derivative mouse embryos and spontaneous abortions in women.
Species: mouse
Mutation name: SCP3-/-
type: null mutation fertility: subfertile Comment:Yuan et al. 2002 found that the absence of synaptonemal complex protein 3 (SCP3) promotes aneuploidy in mice oocytes by inducing defective meiotic chromosome segregation. The abnormal oocyte karyotype is inherited by embryos,which die in utero at an early stage of development. In addition, embryo death in SCP3-deficient females increases with advancing maternal age. SCP3 is required for chiasmata formation and for the structural integrity of meiotic chromosomes, suggesting that altered chromosomal structure triggers nondisjunction. SCP3 is thus linked to inherited aneuploidy
in female germ cells and provides a model system for studying age-dependent degeneration in oocytes.Yuan et al. 2002 report without detailing the fact that male null mice are infertile because their germ cells die around the zygotene stage of meiosis.