Meiosis is the basis of sexual reproduction. In female mammals, meiosis of oocytes starts before birth and sustains at the dictyate stage of meiotic prophase I before gonadotropins-induced ovulation happens. Once meiosis gets started, the oocytes undergo the leptotene, zygotene, and pachytene stages, and then arrest at the dictyate stage. During each estrus cycle in mammals, or menstrual cycle in humans, a small portion of oocytes within preovulatory follicles may resume meiosis.
It is crucial for females to supply high quality mature oocytes for sustaining fertility, which is generally achieved by fine-tuning oocyte meiotic arrest and resumption progression. Anything that disturbs the process may result in failure of oogenesis and seriously affect both the fertility and the health of females. Therefore, uncovering the regulatory network of oocyte meiosis progression illuminates not only how the foundations of mammalian reproduction are laid, but how mis-regulation of these steps result in infertility.
In order to provide an overview of the recently uncovered cellular and molecular mechanism during oocyte maturation, especially epigenetic modification, the progress of the regulatory network of oocyte meiosis progression including meiosis arrest and meiosis resumption induced by gonadotropins is summarized.
Then, advances in the epigenetic aspects, such as histone acetylation, phosphorylation, methylation, glycosylation, ubiquitination, and SUMOylation related to the quality of oocyte maturation are reviewed.
Uncovering the signals involved in controlling the resumption of oocyte meiosis is a major issue in female reproductive biology. The meiosis initiation and resumption of oocytes is different from sperm in at least three aspects. Female germ cells enter and undergo the first meiotic progression during embryonic development, and arrest at the diplotene stage of prophase I before birth. And, some of the arrested oocytes within fully grown follicles will resume meiosis after puberty in response to luteinizing hormones LHs during each estrous animal or menstrual cycle human Mehlmann, Last, the cell division of oocytes is known as asymmetric cytokinesis.
Interestingly, whenever fully grown oocytes are released from follicles and cultured in appropriate medium in vitro , spontaneous resumption happens as well Pincus and Enzmann, Oocyte meiotic maturation is a complicated and vital process used to attain full competence required for the oocyte as well as early embryonic development.
An oocyte arrested at meiotic prophase I contains a large nucleus covered by a nuclear envelope, which is known as the germinal vesicle GV. With the arrival of LH surge, serial processes related to oocyte nuclear maturation, such as chromatin condensation and germinal vesicle breakdown GVBD , occur in oocytes of fully grown follicles.
Later, after extrusion of the first polar body PB1 containing a small portion of cytoplasm, an oocyte containing one set of chromosomes completes meiosis I. Very soon after that, the second meiosis starts and the oocyte mature egg arrests at metaphase II MII until fertilization. Actually, the oocyte accomplishes its meiosis progress only when fertilization happens. In humans and animals, multiple factors including epigenetic molecules and different signaling pathways have been identified and proven to be pivotal for meiotic maturation.
They not only regulate oocytes maturation, but also coordinate with each other to ensure good oocyte quality. This article aims to review the events and development around the quality control of mammalian oocyte meiotic maturation in nuclear and cytoplasm aspects, of which, the underlying molecular mechanisms are discussed to provide detailed information for better understanding of meiosis.
Before an oocyte is enclosed by ovarian granulosa cells to form primordial follicles, meiosis has been initiated and the cell has arrested at the diplotene stage of prophase I Bowles et al. When females are sexually mature, a small portion of primordial follicles will be activated and start to grow gradually. Later, oocytes in fully grown follicles in response to gonadotropins stimulation possess the capability to resume meiosis and ovulate in vivo.
In mammals, meiotic arrest is regulated by a high level of cAMP in the oocyte Conti et al. Therefore, a constantly higher level of cAMP becomes the priority for oocytes to sustain meiosis at the GV stage.
Mice oocytes lacking AC3 expression fail to maintain meiosis arrest Horner et al. Similarly, blocking Gs function causes spontaneous resumption of meiosis in follicle-enclosed mouse oocytes Mehlmann et al.
GPR3, which is located in the oocyte plasma membrane, is necessary to stimulate Gs activity and elevate the level of cAMP Kalinowski et al.
The studies in pig oocytes are consistent with those in mice Yang et al. In a PDE3 knockout model, oocytes are permanently arrested at the GV stage and female mice are infertile Vaccari et al.
Meiosis inhibition is a process in which oocytes coordinate with granulosa cells to sustain a high level of cAMP. Cumulative data have proven that intrinsic cAMP produced by oocyte alone is not sufficient to maintain meiotic arrest.
Besides, NPR2 mutant mice are infertile due to premature resumption of meiosis because of the shortage of cGMP production in CGCs, which results in oocyte fragmentation and poor embryo development Geister et al.
Together, these results suggest that cGMP produced in granulosa cells play a vital role in keeping the cAMP level high in the oocyte, and that maintaining oocyte meiotic arrest requires coordination between granulosa cells and an oocyte within a follicle. In addition, Yang et al. Interestingly, supplementary natriuretic peptide precursor type B NPPB and NPPC are effective at improving the developmental competence of oocytes recovered from small-sized antral follicles of porcine in vitro Zhang W.
As a result, cAMP is degraded and the maturation promoting factor MPF is activated, which induces the resumption of meiosis Norris et al. The regulations of granulosa cells cooperate with oocytes to maintain oocyte meiotic arrest in mice, which are summarized in Figure 1. Figure 1. Schematic model depicting the mechanisms of meiotic arrest.
Meiotic arrest in fully grown oocytes is required by the synthesis and maintenance of high levels of cAMP, the arrest state is maintained by the cooperation of granulosa cells and oocytes in the follicles. Fully grown oocytes in early antral and preovulatory follicles have the capability to resume meiosis before LH surge Holt et al. According to the hypothalamus-pituitary-ovary axis feedback theory, an LH surge in response to a peak estrogen surge initiates oocytes meiosis in vivo through positive feedback regulation.
LH surge produces rapid changes in MGCs via intracellular pathways and extracellular paracrine loops. As a result, the activated LHR induces serial affairs in follicular granulosa cells and oocytes. The mechanism of how high levels of cAMP are necessary to prevent meiotic maturation in oocytes is more or less fully understood. The ability of CDK1 to phosphorylate target proteins at specific serine and threonine residues depends on its activity and binding with the cyclin B Jones, ; Jaffe and Egbert, Besides, CFP1 coordinates histone H3 lysine-4 trimethylation and meiotic cell cycle progression in mouse oocytes Sha et al.
Therefore, one of the key points to initiate oocyte meiosis depends on when to activate CDK1. Conditional deletion of LSD1 in growing oocytes results in precocious resumption of meiosis and spindle and chromosomal abnormalities Kim et al. Synthesis and accumulation of cyclin B1 and its interaction with CDK1 have long been considered prerequisites for oocyte MPF activation as well.
As part of the MPF, cyclin B1 must be constantly degraded by a multi-subunit ubiquitin E3 ligase named the anaphase promoting complex APC to maintain meiosis arrest Jaffe and Egbert, Interestingly, cyclin B1 -null oocytes resumed and finished meiosis I but are then arrested at the meiosis interphase when cyclin B2 is available, indicating that cyclin B2 compensates for the shortage of cyclin B1 in oocyte meiosis I Holt et al.
Gap junction provides a direct communication channel between cells which allow molecules smaller than 1, Da be transferred to the adjacent cells Nicholson and Bruzzone, ; Simon and Goodenough, ; Arroyo et al.
In mice, as many as 20 connexins Cxs participate in forming the channels of the gap junction. Of all connexins, Cx43 and Cx37 are the most studied ones in the follicle and may possess equal importance to folliculogenesis. Ovaries lacking Cx43 do not proceed beyond the primary follicle stage. Also, Cx37, which is mainly expressed between the oocyte and CGCs, is essential to oocyte growth and survival, which in turn is necessary to maintain proper MGC function Li et al.
In Cx37 -knockout mice, folliculogenesis is arrested at the early antral stage and this disruption results in sterility because mutant oocytes grow slowly and cannot survive Carabatsos et al. To examine the roles that Cx37 and Cx43 play in oogenesis, a transgenic mouse model, in which Cx37 specifically replaced Cx43 in growing oocytes, was made. The generations of Cx43 transgene mice driven by zona pellucida 3 ZP3 crossed with Cx37 -null mice are fertile due to the restoration of oocyte—granulosa cell coupling, oocyte growth, and oocyte maturation Li et al.
Thus, despite their different properties, Cx43 may be physiologically equivalent to Cx37 in coupling oocytes with granulosa cells. Both of them are indispensable in the regulation of oocyte maturation.
EGF-related proteins are a set of proteins that respond to the LH signal and promote oocyte maturation. The activation of EGFR is required for oocyte meiotic resumption and cumulus cell expansion Fan et al. Furthermore, in granulosa cell-specific EDFR deleted mice, oocytes cannot resume meiosis Hsieh et al.
Then, cumulus expansion and oocyte maturation starts Wang et al. Recently, Wang et al. In addition, calcium signaling is involved in gonadotropin-induced oocyte maturation in many species Veldhuis, ; Su et al. As a result, cGMP levels and meiotic resumption decreases Hao et al. The regulations of granulosa cells cooperate with oocytes to resume meiosis induced by LH surge in mice, which are summarized in Figure 2.
Figure 2. Schematic model depicting the mechanisms of LH-induced meiotic resumption. As one the key factors that heavily determines the quality of an oocyte, the cytoplasmic maturation of oocytes is critically important, which includes the synthesis, activation, and degradation of maternal mRNA as well as orderly arrangement of organelles Schellander et al.
The expression and degradation of maternal mRNA is developmental stage dependent. Along with the growth of activated follicles, the transcription of genes necessary for oocyte growth and meiosis resumption accumulate and are stored in the cytoplasm. With the initiation of meiotic resumption, not only does the transcription in oocytes cease because of staining agglutination, but the maternal mRNAs stored in oocytes are degraded and gradually consumed.
As to protein synthesis, although a large amount of maternal mRNA exists in fully grown oocytes at the GV stage, they are translationally dormant in mice until meiotic maturation Piccioni et al.
The freshly translated proteins after oocytes resume meiosis play important roles in meiotic spindle assembly, MII arrest maintenance, and mRNA clearance during maternal zygotic transition MZT Walser and Lipshitz, Generally, novel mRNA synthesis is initiated in the late stage of fertilized eggs Piccioni et al. Actually, the degree of polyadenylation of mRNA affects oocyte translation activation as well. Cytoplasmic polyadenylation is a key process that serves to unmask particular mRNAs and enables them to be translated Richter, ; Ivshina et al.
In its simplest form, masked mRNA refers to dormant transcripts in the oocyte that are to be translated during completion of meiotic divisions or in early embryos. The degradation of maternal mRNA is controlled strictly in oocytes undergoing meiotic resumption and in early embryos.
In mouse oocytes, transcriptional destruction, especially the transcripts of oxidative phosphorylation, energy production, and protein synthesis during the transition from GV to MII, is selective rather than promiscuous. It is stated that the selective degradation of the transcription of maternal mRNAs is a prerequisite for the activation of the zygotic genome Su et al. Particularly, regulation of maternal mRNA translation and degradation mainly occurs in maturing oocytes rather than in fertilized eggs, but these mechanisms are essential for the oocyte and zygote to build up competence to accomplish MZT.
The starting point of the MZT is oocyte activation from meiotic arrest rather than fertilization Sha et al. In the major pathway of mRNA degradation, shortening of the poly A tail, or deadenylation, is the first and rate-limiting step Walser and Lipshitz, For instance, meiosis arrest female 1 MARF1 is an essential regulator of important oogenic processes leading to female fertility and the development of healthy offspring by suppressing levels of specific transcripts Su et al. The cytoplasmic maturation of oocytes also includes the maturation of various organelles, especially cortical granules, mitochondria, the endoplasmic reticulum ER , and cytoskeleton.
The time dependent distribution and structure of these organelles are indispensable for the respective functions. Cortical granules are membranous organelles derived from Golgi complexes, which are found in the cortex of unfertilized oocytes Liu et al.
Besides, mitochondria are the key to ATP energy supply in oocytes. Impaired oocyte quality, including meiosis chromosome separation, maturation, and fertilization failure, correlates with both abnormal mitochondrial rearrangement and low ATP level Blerkom, ; Dumollard et al. Since the cytoskeleton is mainly composed of microtubules and filaments and the recombination of spindles is strictly controlled by the microfilament network Verlhac et al.
Multiple posttranslational modifications exist in developing oocytes, including acetylation, phosphorylation, methylation, glycosylation, ubiquitination, and SUMOylation of various proteins Allfrey et al. As follows, the changes and regulation as well as functions of histone modifications during meiotic maturation of mammalian oocytes, with particular emphasis on histone acetylation and methylation are summarized.
Contrarily, deacetylation is associated with transcriptional inactivation. In mammals, as many as 18 HDACs are identified and divided into four classes based on their homology with yeast proteins Bolden et al. The respective actions of these proteins in oocytes are reviewed in the following. HDAC1 in the nucleus decreases gradually during the growth of oocytes and co-localizes with chromosomes following meiosis resumption.
In contrast, HDAC2 in the nucleus increases between 5 and 12 days post-partum, and is relatively stable during the growing period of mice oocytes. The low level acetylation of H4K16 is essential for the function of centromeres. Interestingly, the deletion of maternal HDAC2 caused high level acetylation of H4K16 and resulted in disorder in chromosome segregation and kinetochore function during MII in oocytes Ma and Schultz, HDAC3 is expressed in the nucleus of GV oocytes and disperses in the cytoplasm of oocytes after meiotic resumption.
HDAC3 also has functions in promoting meiotic apparatus assembly in aging mouse oocytes. The above results indicate that HDAC3 in both granulosa cells and oocytes plays important regulatory roles in oocyte maturation. HDAC8 could be important for oocyte maturation according to its distribution in growing oocytes. It is widely distributed in the cytoplasm of mouse oocytes at the GV stage.
Inhibition of HDAC8 in fully grown oocytes causes spindle defects and chromosome misalignment during oocyte meiotic maturation, accompanied by impaired kinetochore-microtubule attachments Zhang K. Conditional deletion of HDAC8 by Vasa -Cre results in subfertile females, which is independent of chromosome segregation errors during meiosis Vijay Pratap et al.
On the whole, HDAC8 is important for oocyte development and maturation, but the mechanisms of its action on oocytes needs further study. According to existing reports, the expression of HDAC4 is maintained at a high level in fully grown oocytes until the MII stage, and then dramatically decreased after fertilization, it may play specific roles during mouse oocyte maturation Kageyama et al.
Overexpression of HDAC6 results in GV oocytes and pronuclear zygotes which results in altered nuclear structure and causes compaction of the chromatin Verdel et al. Sirtuins are generally important for oocyte development. Activation of SIRT1 by resveratrol in vitro improves oocyte quality and embryo development in mice, pigs, and cows Liu et al.
SIRT1 relates to mitochondria biosynthesis and degradation in oocytes because resveratrol supplementation improves the mitochondrial function and the developmental capability of the oocytes Sato et al. Last, SIRT6 is important in regulating meiotic progression as well. Depleted SIRT6 results in disruption of spindle morphology and chromosome alignment in oocytes Han et al. Inhibition of HDAC11 by JB significantly interrupted mouse oocyte meiosis progress, possibly because of abnormal spindle organization and misaligned chromosomes, impaired kinetochore-microtubule attachment, and spindle assembly checkpoint function Sui et al.
Importantly, K lysine acetyltransferase 8 KAT8 is a highly conserved MYST family member who is specifically responsible for H4K16 acetylation and is important for mouse oocyte development, by regulating reactive oxygen species levels Thomas et al. The protein is mainly located in the nucleus throughout the growth phase, but upon GVBD, the staining intensity decreases and the signal becomes uniformly dispersed throughout the oocyte.
Oocyte KAT8 deletion results in female infertility with defects in follicle development and increased oocyte apoptosis Yin et al. It concentrates in the vicinity of the meiotic spindle rather than on chromosomes in the MI stage Champagne et al. Histone acetyltransferases p and the CBP subfamily are constitutively expressed in the GCs of growing and ovulatory follicles in a gonadotrophin-independent manner.
Taken together, HATs have essential roles in mouse follicle development and oocyte maturation, and the potential functions of HATs in oocytes maturation needs more exploration. Histone methylation correlates with chromatins activity. For instance, H3K4 methylation is associated with the activation of chromatins and occurs mainly in the promoter regions of active genes, while the methylations of either H3K9 or H3K27 relates to gene inactivation Werner and Ruthenburg, In developing mouse oocytes, the level of H3K4me3 are elevated during the transition of chromatin configuration from the non-surrounded nucleolus NSN to surrounded nucleolus SN type Yu et al.
Histone methylation modification is regulated by histone lysine methyl transferases KMTs and histone lysine demethylases KDMs via modifying lysine residues and the number of methyl groups Sha et al.
And the oocytes as well as zygotes display perturbed cytoplasmic organelles and aggregated lipid droplets Brici et al. Loss of KMT2B in mouse oocytes induced by GDF9 -Cre resulted in abnormal meiosis maturation, anovulation, oocyte death, and female sterility, in which H3K4 level decreased and gene expression was abnormal Andreu-Vieyra et al. KDM1B is highly expressed in growing oocytes and the level persists through later stages of oogenesis, but it is hardly detectible in oocytes of primordial and primary follicles in mice.
The deletion of KDM1B in mice does not affect embryo development, animal survival, or oocyte growth. Early embryos derived from these oocytes show biallelic expression or suppression of the affected genes and died before mid-gestation Ciccone et al. KDM4A is the major demethylase functional in MII oocytes and is required to maintain the genomic stability of pre-implantation embryos Sankar et al. Protein phosphorylation occurs most often on serine, threonine, or tyrosine residues and competently regulates cell cycle stage-related affairs in a variety of different signal transduction pathways Schatten and Sun, For example, histone H3 phosphorylation at Ser10 and Ser28 affects chromatin condensation of either mitosis or meiosis Bradbury et al.
In addition, protein phosphatase 1 PP1 dephosphorylates H3 at Ser10 in budding yeast and nematodes. Taken together, the balance of Aurora B kinase and PP1 activities regulate the meiotic phosphorylation of histone H3 in mammalian oocytes.
Importantly, APC initiates the metaphase to anaphase transition by inducing the degradation of cyclin B and securin Jones, Also, protein ubiquitin Ub E3 ligases trigger specific protein degradation and thus plays an important role in the process of both the meiotic and mitotic cell cycle Huo et al. Interestingly, cullin ring-finger ubiquitin ligase 4 CRL4 is one of E3 ligase members who exert multiple functions in the maintenance of oocyte survival and meiotic cell cycle progression Jones, Deletion of DCAF13 in oocytes resulted in not only decreased CDK1 activity and impaired meiotic cell cycle progression as well as chromosome condensation defects, but also polyubiquitination and degradation of PTEN Zhang et al.
In addition, protein-ubiquitination mediated CCNB1 and securin degradation is essential for the metaphase to anterograde transition during oocyte meiotic maturation Herbert et al.
UCHs present in oocytes in many species. UCHs have a complimentary distribution in porcine, bovine, and murine oocytes. UCHL1, one of the most abundant proteins in mammalian oocytes, accumulates in the oocyte cortex.
UCHL3 is associated with oocyte spindle Mtango et al. Inhibiting UCH activity causes excessively large PB1, distorts the meiotic spindle, and disrupts other spindle attributes, such as chromosome alignment Mtango et al.
In follicular granulosa cells, the ubiquitin-proteasome system UPS was involved in regulating the deposition of the extracellular matrix of cumulus and steroidal formation during the expansion of cumulus cells, implying that this system may be pivotal for follicle development Nagyova et al. Protein glycosylation is one of the most frequent post-translational modifications PTMs , which affects many things, such as protein folding, distribution, stability, and activity.
There are two main types of glycosylation in cells, N-linked and O-linked glycosylation Ohtsubo and Marth, Defects in the process of protein glycosylation leads to many clinical diseases. Protein N -glycosylation in oocytes is crucial for female fertility. DPAGT1 missense mutation causes subfertility in females due to defective follicular development and less ovulation Li et al. Also, due to the decreased glycosylation of ZP proteins, the mutant oocytes have a thin and fragile ZP layer and have poor developmental ability after in vitro fertilization.
Furthermore, the first meiotic division is accelerated in such mutant oocytes. Importantly, the phenotypes of conditional knockout of DPAGT1 in infertile mouse oocytes is consistent with those in humans Li et al.
Protein O -glycosylation plays a small role in oocyte maturation. Glucosamine treatment during in vitro maturation does not affect the meiotic maturation of cow, pig, or mouse oocytes, but blastocyst development was severely inhibited Schelbach et al. This suggests that protein O -glycosylation does not affect oocyte maturation, but it affects the quality of oocytes.
UBE2I primarily expresses in the nucleoplasm of mouse growing oocytes at least from postnatal day 13 to GV-stage fully grown oocytes. UBE2I is downregulated following meiotic resumption Ihara et al.
The importance of SUMOylation on oocytes maturation could be highlighted by the following facts. After endogenous SUMO1 or UBC9 activities in oocytes were either inhibited or silenced, the percentage of GVBD and PB1 extrusion was significantly reduced, together with abnormal spindle organization, chromosome misalignment, segregation defects, and aneuploidy in matured oocytes Yuan et al.
Similarly, inhibition of UBE2I for GV-stage mouse oocytes disrupts meiotic maturation and causes defects in spindle organization Yuan et al. Deletion of UBE21 by GDF9 -Cre results in complex infertility phenotypes, including defects appearing at multiple critical oocyte transition points, such as unstable ovarian reserves, impaired communication with granulosa cells, and defective resumption of meiosis and meiotic progression Rodriguez et al.
Other proteins that affect oocyte maturation are also involved in the process of SUMOylation. Oocyte maturation is a complex process involving multiple steps and is regulated by many molecules and signaling pathways. In recent years, due to the rapid development and popularization of technologies like the genetic modification of animal models, molecular biology, and biochemistry, researchers have gained a better understanding of oocyte GV arrest and meiosis I resumption.
The major cellular and molecular affairs, especially the epigenetic modification events related to oocyte maturation in response to hormone induction, and the major advances in this field, are highlighted in this review. Since the development of an oocyte depends not only on the oocyte itself, but on mutual communication and physical contact with follicular granulosa cells, it is important to focus more on epigenetic changes within oocytes, ovarian granulosa cells in response to hormones, and other extracellular molecules induction.
Besides, applying microscopes with high resolution and a high-throughput analysis technique, such as mono-cellular based sequencing and omics techniques, should be emphasized to present clearer 3D or even time-dependent 4D representations of critical affairs that happen during oogenesis.
Finding more specific oocyte-expressed proteins, such as RBPs and oocyte-derived paracrine molecules, may contribute to uncover the mysterious mechanisms of oocyte meiosis as well. Further, integration of analysis of sequencing data, comparing the data collected from different breeds, and verifying the function of each individual molecule in vitro and in vivo simultaneously based on multiple animal models are also plausible. MH and TZ collected the information and wrote the manuscript.
CW and YY revised the manuscript. All authors read and approved the final manuscript. The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
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Reproduction , — Bobrowska, A. PLoS One 6:e However, it is not completely random. It is all based on the original genetic material the embryo received from its father and mother. These cells continue to multiply until reaching their peak. The peak occurs when the developing fetus is about five-months-along. At this point, the girl fetus has 7 million oocytes. This number will begin to decrease after this point. At birth, a baby girl has only 2 million oocytes left. Every oocyte will go through two separate meiotic cell divisions before becoming a mature ovum.
Meiotic cell division leads to growth and maturity of the oocyte, and not additional oocytes. Towards the end of prenatal development, the oocytes stop multiplying in number and begin to mature individually. At this stage, they go through the first meiotic cell division. This cell division leads to oocyte growth—not more oocytes—like what happens with the oogonium.
The primary oocytes freeze in their development and remain frozen until reproductive hormones trigger the next stage. Oogenesis will continue at the age of puberty. Puberty jump-starts the next stage of oocyte maturity. Not all the oocytes will go through these later stages of oocyte development together, of course. Each month, a new set of primary oocytes begin to mature.
Once a primary oocyte is affected by reproductive hormones, it completes Stage I of the meiotic cell division. This is known as oocyte maturation. At the end of this first stage of meiotic cell division, the cell splits into two separate cells: a small polar body and a large secondary oocyte. The small polar body eventually deteriorates. The secondary oocyte begins the next stage of maturation. The oocyte now begins the second phase of meiotic cell division.
Eventually, the secondary oocyte will split again into two separate cells: another small polar body cell and a larger mature cell. This larger mature cell is known as an ootid.
As before, the smaller polar body cell will eventually deteriorate. Ovulation occurs when the oocyte has reached the ootid stage of development. At the time of ovulation, an ootid is released from the follicle. Human egg cells cannot move on their own. Instead, finger-like projections draw the oocyte towards and into the fallopian tube.
Once inside the fallopian tube, small hair-like projections known as cilia continue to draw the ootid along. In the fallopian tube, if pregnancy occurs, the ootid is fertilized by a sperm cell. Once this fertilization takes place, the ootid goes through its final stage of maturation and becomes an ovum, a fully mature human egg cell.
During fertilization, the ovum and sperm cell combine, each containing 23 chromosomes each. Rather quickly but not at the exact moment of fertilization , these chromosomes fuse together, creating a new cell with a full set of chromosomes.
This new cell is called a zygote. The zygote will develop into an embryo and, about nine months later, a newborn baby. Get diet and wellness tips to help your kids stay healthy and happy. Female age-related fertility decline. Committee Opinion No. Fertil Steril. History and challenges surrounding ovarian stimulation in the treatment of infertility. Ovarian hyperstimulation syndrome. Females are not capable of making new eggs, and in fact, there is a continuous decline in the total number of eggs each month.
Over the next years of a female's reproductive life, the entire egg supply will be depleted. Although no one can know with absolute certainty the number of eggs remaining within the ovaries at any given time, most women begin to experience a significant decrease in fertility the ability to conceive a child around the age of At the time of menopause, virtually no eggs remain.
The large supplies of eggs within each ovary are immature, or primordial, and must undergo growth and maturation each month. The eggs are stored within follicles in the ovary.
Within a woman's lifespan, large numbers of follicles and oocytes will be recruited to begin the growth and maturation process. The large majority, however, will not reach full maturity.
Most will die off in a process called atresia. Thus, only about of these eggs will mature over a women's life span. The maturation of eggs typically takes about 14 days and can be divided into 2 distinct periods.
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