#diplotene stage

[starlighttaylorsversion]

My legs felt like jelly after i rode bicycle for like 20-25 mins, and then my periods arrived. WHY DO PERIODS EVEN EXIST, i know its important , but the first day of mensuration is fricking fricking painful. ugh anyways, pls tell me i should be motivated enough, for my 5'1 52 kg body to continue cycling🙂

[geneticteacher123]

Meiosis one is the first divisions of meiosis like mitosis have 4 stages (Prophase 1, Metaphase 1, Anaphase 1 and Telophase 1) that forms two daughter cells. In Prophase 1, homologues pairs of chromosomes are tangled together by a process called crossing over and spindle fibers and centrioles appear. In Metaphase 1, homologous pairs of chromosomes line up next to each other along the equatorial plate. Whereas, in Anaphase 1, spindle fibers pull homologues chromosomes apart. Meanwhile, in Telophase 1 and Cytokinesis 1, nuclear membrane and two new haploid daughter cells are formed. In addition, the Prophase one substages are: 1- Leptotene, chromosomes become start to condense, 2- Zygotene, homologues chromosomes become closely associated (synapsis) to form pairs of chromosomes (bivalent) consisting of four chromatids (tetrad), 3- Pachytene, crossing over of non-sister chromatids of homologues chromosomes occurs at recombination nodules and the chromosomes remain linked at the sites of crossing over to form chiasmata, 4- Diplotene, homologues chromosomes start to separate but remain attached by chiasmata, 5- Diakinesis, homologues chromosomes continue to separate and chiasmata move to the end of the chromosomes #geneticteacher

[juniperpublishers-gjorm]

Oocyte Quality and Female Infertility

Abstract

Female infertility is one of the major reproductive health issue affecting majority of women worldwide. Several factors including environmental, hormonal and physical may affect the physiology of ovary to release quality grade oocyte required for fertilization and early embryonic development. The quality of oocyte is dependent on several factors within the follicular microenvironment and even after ovulation. One of the major factors that affect oocyte quality is the induction of apoptosis. Apoptosis plays a major role to eliminate majority of germ cells from the cohort of ovary during various stages of folliculogenesis. Few numbers of oocytes are selectively recruited to get ovulated during entire reproductive life span in female. Prior to ovulation, these oocytes achieve meiotic competency that may last for several months in rodents to several years in human. Inability to achieve meiotic competency within the follicular microenvironment and spontaneous egg activation (SEA) immediately after ovulation may deteriorate oocyte quality. Thus, induction of apoptosis or meiotic arrest at Metaphase-I stage (M-I) or SEA could reduce female fertility and may cause infertility.

Keywords: Apoptosis; Oocyte competency; Spontaneous egg activation; Ovary; Female infertility

Abbreviations: SEA: Spontaneous Egg Activation; M-I: Metaphase-I; M-II: Metaphase-II; M-III: Metaphase-III; PB-I: First Polar Body; PB-II: Second Polar Body; ROS: Reactive Oxygen Species

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Introduction

Infertility is a one of the major reproductive health problems that has affected almost 10% of young age group worldwide. The infertility rate remains unchanged over past two decades besides having significant advancement in reproductive health sector [1]. This could be due to environmental, stress, lifestyle factor, hormonal and pathophysiological factors [2]. These factors directly or indirectly affect the physiology of ovary that is responsible for the generation of competent oocytes for fertilization and early embryonic development [3]. The increase of stress hormone induces granulosa cell apoptosis responsible for synthesis of estradiol-17β. Estradiol depletion at the level of ovary affects follicular growth and development [2]. Amelioration in follicular growth and development induces follicular atresia [4]. The increased stress causes oxidative stress and reactive oxygen species (ROS) at the level of ovary trigger germ cell depletion via apoptosis [5]. Several factors and pathways facilitate germ cell depletion at all the stages of oogenesis in mammals [6]. The large number of germ cells is eliminated from the cohort of ovary just before the attainment of puberty [4]. At puberty, less than 1% of germ cells remains in the ovary that are subjected to selective recruitment process during entire reproductive life span [7].

The selective recruitment of oocytes during puberty in response to pituitary gonadotrophin surge induces meiotic resumption from diplotene arrest in follicular oocytes by increasing the level of cyclic nucleotides as well as Mos level in granulosa cells of follicular oocytes [8]. These cyclic nucleotides and MOS/MEK/MAPK signalling pathways disrupt the gap junctions between granulosa cells and oocytes resulting in a transient decrease of oocyte adenosine 3',5'-cyclic monophosphate (cAMP) required to maintain diplotene arrest in follicular microenvironment [9]. A transient decrease of oocyte cAMP activates mitogen-activated protein kinase (MAPK) as well as cyclin dependent kinasel (Cdkl), a catalytic unit of maturation promoting factor (MPF). Further, decrease of cAMP destabilizes MPF [10]. The MPF destabilization causes meiotic resumption from diplotene arrest and oocyte progresses towards to metaphase-I stage (M-I) [11]. The M-I arrest may last for very short period of time in vivo and oocyte progresses to reach metaphase-II stage (M-II) by extruding first polar body (PB-I) at the time of ovulation [12]. However, removal of oocyte from follicular microenvironment and their culture in vitro results in spontaneous resumption of meiosis but they are unable to progress beyond M-I under in vitro culture conditions [13].

These oocytes are unfit for fertilization as they contain diploidset of chromosomes and do not posses PB-I. Further, growing body of evidences suggest that the oocytes after ovulation do not wait for fertilizing spermatozoa and quickly undergo meiotic exit from M-II arrest so called spontaneous activation in several mammalian species [14,15]. The spontaneous activation is possibly due to premature release of calcium (Ca++) from internal stores and increase of cytosolic free calcium. A moderate increase of cytosolic free calcium triggers downstream pathway to destabilize MPF [16]. MPF destabilization results spontaneous activation by initiating the extrusion of second polar body (PB-II). These oocytes are of poor quality and their use limits reproductive outcome and may trigger infertility problems [17].

Apoptosis and oocyte quality

Apoptosis plays a major role in follicular atresia and eliminates majority of defective as well as surplus germ cells from the cohort of ovary [18,19]. By this way, ovary keeps only few numbers of germ cells (less than 1%) for selective recruitment during entire reproductive lifespan. As the aging occurs, decline of number of follicles below threshold level may cause infertility [20,21]. Studies suggest that the good quality of oocyte is ovulated first and as the maternal aging occurs, poor quality oocytes are remained in the ovary. These oocytes are more fragile and susceptible towards apoptosis that reduces reproductive outcome (Figure 1) [22-24]. Women are more frequently exposed to various kinds of stress during their reproductive period [25]. The psychological stress, lifestyle changes and various other factors stimulate the release of stress hormone and reactive oxygen species (ROS) [2]. The increased level of stress hormone and ROS induce apoptosis not only in granulosa cells but also in follicular oocytes [5,26]. There are several players and both as death receptors as well as mitochondria-mediated pathways involved in oocyte apoptosis within the follicle of the ovary [27,28]. Indeed, apoptosis plays a major role in determining the quality of follicular oocytes that directly affects reproductive outcome of a female and induces infertility [4].

Meiotic maturation arrest and oocyte quality

Meiotic maturation is required for the follicular oocytes to achieve developmental competency [29]. The achievement of meiotic competency starts with the resumption from diplotene arrest in follicular oocytes and ends with extrusion of PB-I [16]. Any defect during the achievement of meiotic competency does not allow the follicular oocyte to progress meiosis [30]. These compromised oocytes are arrested at M-I stage and do not progress to extrude PB-I [12,13,31]. Further, M-II arrested oocytes even after insemination do not get activated [32]. These oocytes are of poor quality due to meiotic maturation arrest either at M-I stage or at M-II stage under in vitro culture conditions (Figure 1B) [3,33]. The meiotic maturation failure could be possibly due to maintenance of high level of stabilized MPF. The high level of stabilized MPF is required for the maintenance of meiotic arrest [34,35]. The meiotic maturation arrest may cause infertility in human [3].

Spontaneous activation and oocyte quality

The oocyte after ovulation are generally arrested at M-II stage and posses PB-I in most of the mammalian species [3538]. Growing body evidences suggest that oocyte do not wait for fertilizing spermatozoa and quickly undergo spontaneous exit from M-II arrest in several mammalian species including human [39-42]. The initiation of extrusion of PB-II starts but never gets completely extrude (Figure 1C). Oocytes are further arrested at Metaphase-III (M-III) like stage [43].The SEA could be due to abortive increase of cytosolic free calcium and activation of downstream pathway to destabilize MPF [37,38,44]. A moderate increase of cytosolic free Ca++ is good enough to trigger SEA but not sufficient to induce full activation process [37,44]. These oocytes are not fit for fertilization since the chromosomes are scattered throughout the cytoplasm. A large amount of cytoplasm goes towards the side of polar body formation but PB-II never completely extruded [11]. These oocytes are of poor quality and cannot be used for any assisted reproductive technology (ART) program including somatic cell nuclear transfer program (SCNT) during animal cloning [36,11].

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Conclusion

Good quality of oocytes is the right choice for fertilization and early embryonic development. Deterioration in oocyte quality may occur due to the onset of apoptosis in the follicular oocytes. Majority of oocytes are eliminated from ovary via apoptosis during follicular atresia. Only few oocytes remain in the ovary that are selectively recruited for ovulation during entire reproductive life of a female. Prevention of MPF destabilization may cause meiotic maturation arrest in follicular oocytes. After ovulation, oocyte quality undergoes Ca++ mediated MPF destabilization that causes SEA in several mammalian species including human. Thus, apoptosis in oocytes, meiotic maturation arrest and SEA may deteriorate oocyte quality after ovulation. Poor quality oocyte directly impacts the reproductive outcome and causes female infertility.

[themedicineprof-blog]

Embryology 9/12/2017

chromosomal abnormalities. trisomy is an extra chromosome and monosome missing 1 chromosome. ie there should be chromatids that form a chromosome. if 3 single chromatid chromosomes join together instead of the usual 2, this is called trisomy, and if one chromatid does not meet with a second to form a 2chromatid chromosome this is monosomy. the 3 mentioned trisomy defects are numbered by which chromosome it would affect when you do that thing that spreads them out acording to acidity or whatever that experiment you did in biomolecular science class. so trisomy 21 is downsyndrome, trisomy 12 is patau syndrome, and trisomy 18 is edward syndrome. there is another syndrome that is sex dependent that he rapidly mentioned which was klinefelter vs turner syndrome. please check these out before the exam. the teacher starting talking about oogenisis. he said diploid 2n23 before meiosis 1, then meiosis 1, then halploid n23. then meosis 2 for a total of 4 cells. after a female is 35-40 y/o the rate of chromosomal abnormalities drastically increases. and requires charyotyping to check the chromosomes. this method is called FISH and that stands for something i forget. this is performed via aminocentesis? or draining a bit of fluid from the amniotic sack. this works because their is DNA is skin cells. and because the fetus’s skin isnt fully developed some of the skin cells are freerly floating in the amniotic fluid.  the tip of the chromosome is the telomere. the 4 subsections that i mentioned from yesterdays class, little zebras play dominos was the correct lettering and those letters stand for leptotene, zygotene, pachytene, and diplotene. spermatogenisis starts at puberty unlike oogenisis which starts intrauterine life of the fetus. it starts at the 3rd month of pregnancy and ends at 7 months. next the teacher outlined major steps of spermatogenisis.  oogenisis ends at the end of phrophase 1 at end of the diplotene step and does not continue like spermatogenisis. the oocytes remain dormant from the end of diplotene and stay dormant until puberty.  ampulla means dialated and is the largest part of the fallopian tube which is right outside the ovarie with the fibere, or finger like projections. the istimus is the narrowest part of the fallopian tube and is the area that attaches to the uterus. the uterus has 3 layers and the teacher told us to concentrate on the innermost layer because that is the ‘functional layer.’ its the layer that swell, sheds, the placenta attaches too, its the functional layer. its highly vascular with an embomidral glands? the internal os vs the external os is the opening of the cervix and internal is inside the uterus, external closer to the vaginal canal. next he reviewed the menstral cycle which totals 28 days. the first stage is the follicular, goes from 1-14 and includes menses which is days 1-5. then the 2nd stage is the luteal phases which occurs between days 14-28? theres a gap in there somewhere? and this all needs to be clearified and studied before the test. the corpus leutium gives meaning to the luteal phase. its an empty follicule? and secretes progesterone. progesterone maintains proliferated endomyetrium. the corpus letium releases progesterone for 3 monts if fertilization occurs, but then from 3-9 months the placenta takes over the release of progesterone. i am unsure but if i remember right from nursing school i am pretty sure the corpus leitium becomes the placenta? idk remember to lookup placenta’s origin of creation.

[shimashimashippo]

on menstruation & ovulation

hello friends, i’m currently reading some articles [1][2][3] and here are my notes along the way (because it’s very easy to confuse what does what and all that jazz). 

(disclaimer: i’m doing my best to write / explain this simply. it’s pretty long and also just my understanding of the articles. please feel free to correct me if you feel i have misunderstood something. i definitely encourage you to read the linked articles yourself! [numbers] are links to articles / [x] are links to pictures & diagrams.)

for a general overview [1], i’d like to start by saying that the menstrual cycle is usually 28 ± 3 days long. those whose cycles are < 21 days are called “polymenorrheic,” while those whose cycles are > 35 days are called “oligomenorrheic.”

it involves both the ovarian cycle and the uterine cycle and can be divided into two phases, whose names depend on which cycle (ovarian / uterine) you’re talking about. i’ll mostly be using “follicular” and “luteal” from the ovarian cycle.

ovarian: (1) follicular phase / (2) luteal phase

uterine: (1) proliferative phase / (2) secretory phase

ovulation (release of an oocyte / egg) happens right smack in between the two phases, which are usually approximately equal in length (14 days each).

but let’s first go over the key regulatory factors [1] in all of this briefly! you first have your hypothalamus producing gonadotropin releasing hormone (GnRH / sometimes called gonadotropin-releasing factor) which causes the anterior pituitary to produce two gonadotropins (basically glycoprotein polypeptide hormones, according to wikipedia), follicle stimulating hormone (FSH) and luteinizing hormone (LH). these two gonadotropins (FSH & LH) then go on and stimulate the ovaries to produce estrogen, progesterone along with some other kinds of signaling peptides. the ovarian steroids (estrogen & progesterone) stimulate endometrial (uterine lining) growth / proliferation (this will be discussed later in more detail).

∴ GnRH (hypothalamus) → FSH & LH (anterior pituitary) → estrogen, progesterone & friends (ovaries & follicles) [x]

let’s talk a bit about oocyte and follicle development / growth [2][4]. 

if you remember from my last post on oogenesis [here], while the oocyte is still in dictyate / diplotene of prophase I, it is enveloped in a primordial follicle which consists of a layer of granulosa cells and another layer of thecal cells, with the granulosa cells being the closer of the two to the oocyte. [x] 

in folliculogenesis, FSH is a key player since it stimulates...

the original primordial follicle to grow and become capable of developing into an antral follicle 

the production of FSH receptors (so that it will be receptive to the FSH surge in the follicular phase) on granulosa cells and of aromatase (which converts androstenedione and estrone into estrogen)

the production of estrogen

#2 and #3 along with the interactions between the granulosa and thecal cells makes for very high levels of estrogen, which stimulates the follicle to grow even more but suppresses the production of FSH.

in the meanwhile, the granulosa cells also proliferate with the growing oocyte to create several layers, the innermost of which will remain with the oocyte even when it is released into the oviduct to be fertilized (or not) and is called the cumulus. in the meanwhile, as the follicle continues to grow, so does an antrum (cavity) between the follicle surface and the oocyte, to be filled with proteins and hormones among other molecules. [x]

the oocyte and follicle also encourage each other to grow as well ー the oocyte secretes paracrine factors while the follicle secretes growth and differentiation factors (TGF-β2, VEGF, leptin, FGF2). those secreted by the follicle also help direct blood vessels towards it.

after some time, a dominant follicle must be selected. usually it’s a matter of timing ー the oocyte & follicle pairing in the right stage of development just as the gonadotropins (recall FSH & LH) rise survives.

after all of that background information, we can now discuss the actual processes of menstruation & ovulation... 

in the follicular phase, the pituitary gland begins secreting a lot of FSH, which stimulates maturing follicles that have already reached a certain stage in their development to grow even more, along with granulosa cells to produce more LH receptors. shortly thereafter, the pituitary starts secreting LH which breaks the oocyte out of its dictyate state to push it through meiosis I. recall that through asymmetrical division, this results in one secondary oocyte and one polar body ー both of which are encased in the zona pellucida that was being transcribed and produced during diplotene. it is here that ovulation begins.

the production of FSH & LH induces the production of estrogen (among other things) which has the following five effects:

it stimulates the endometrium (uterine lining) to grow and to become “enriched with blood vessels”

it decreases the amount of cervical mucus and therefore the possibility of sperm getting stuck in said mucus while they’re on their mission in the reproductive tract in search of the egg

it causes the granulosa cells of mature follicles to produce more FSH receptors and the hormone inhibin which causes a decrease in production of FSH by the pituitary

the concentration / production of estrogen is directly proportionate to the production of LH (more estrogen = more LH / less estrogen = less LH)

however, at very high concentrations and for long durations, it stimulates the hypothalamus to produce GnRH ∴ ↑ estrogen = ↓FSH & ↑ LH  

nearing the end of the follicular phase, the level of estrogen peaks followed by a a huge burst in LH and a small burst in FSH. 10-12 hours after the gonadotropin peak, the egg is finally released. such is the beauty that is ovulation.

now we enter the luteal phase. the now hollow follicle becomes is called the corpus leutum under the continued production of LH. (the previous surge in FSH stimulated growth in more LH receptors; thus allowing them to continue being sensitive to LH levels.) the corpus leutum begins secreting mostly progesterone along with a bit of estrogen. 

progesterone plays two important roles:

stimulates the growth / development / thickening of the endometrium to prepare it for implantation by the fertilized egg (if it ever gets fertilized). 

 inhibits the production of FSH and thereby the maturation of any other follicle & egg pair, because there can only be one per cycle. (fun fact: this is why birth control is often a combination of estrogen and progesterone. both work together to suppress / inhibit FSH and typically result in delaying / inhibiting ovulation.)

(in case you’re confused and lost with all the hormones, i’ve drawn a little flow-chart-type thing [x])

but what happens to the egg / oocyte?

it does not get fertilized ー no big deal. both the corpus leutum and endometrium deteriorate away and progesterone levels drop; thus allowing FSH to rise as the cycle restarts.

it get fertilized ー it goes from a two-cell embryo which divides to become a morula and eventually to a multicellular blastocyst. the outer layer of the blastocyst, called the trophoblast, secrets luteotropin which maintains the corpus leutum and the high levels of progesterone. and then pregnancy happens.

so there you have it! i’ll be talking about fertilization in more detail next time. if you have any questions, let me know and i’ll do my best to answer them! 

that is all for now!

oogenesis & spermatogenesis // menstruation & ovulation // fertilization

[simplifiedbiology-blog]

New Post has been published on https://ramneetkaur.com/cell-division-mitosis-meiosis/

Cell Division - Mitosis & Meiosis

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CELL DIVISION: Mitosis & Meiosis

Cell Cycle

Can be divided into 2 stages: INTERPHASE.

G1 Growth phase 1.

S  Synthetic phase.

G2 Growth phase 2.

DIVISIONAL PHASE.

M Mitosis/Meiosis.

C Cytokinesis.

Mnemonic:“Go Sally Go! Make Children!”

  Mitosis

It is an equational division. Occurs in somatic cells.

Prophase, Metaphase, Anaphase, Telophase

Mnemonic: “People Meet And Talk”

Prophase:

Coiling of chromatin occurs, forming thin long threads.

By the end, chromosomes start forming,

Nucleolus & nuclear membrane starts disappearing by the end.

Spindle fiber formation starts.

Centriole in animal cells starts moving towards the poles.

Metaphase:

Nuclear membrane and nucleolus has disappeared,

Spindle fibers have formed, 

2 types of spindle fibers occur chromosomal fibers that are attached to chromosomes at the centromere & continuous fibers that join the 2 poles.

Chromosomes having two chromatids are seen,

Chromosomes align themselves on the equatorial plate due to contraction of spindle fibers.

Amphiastral mitosis occurs in animal cells & anastral mitosis occurs in plant cells.

Anaphase:

Shortest phase.

Centromere splits

Chromosomes start moving towards poles due to contraction of spindle fibers.

Various shapes of chromosomes are seen.

Telophase:

Chromosomes have reached the poles,

Uncoiling of chromosomes occur,

Nucleolus and nuclear membrane reappear,

Spindle fibers disappear.

2 nuclei are formed by the end.

Cytokinesis:

Starts in mid-Anaphase and ends by the end of Telophase dividing the cell into 2 daughter cells.

Occurs by invagination of the cell membrane in animal cells & by cell plate method in plant cells.

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Meiosis

It occurs in 2 stages:

Meiosis I – reductional division:

Prophase I, Metaphase I, Anaphase I, Telophase I.

Prophase I: divided into 5 substages.

Mnemonic: Little Zara in Pink Dress is Dancing.

Leptotene:

Chromatin coils forming thin long threads.

Zygotene:

Further coiling of chromatin occurs.

Pairing of homologous chromosomes occurs due to the mutual attraction between them.

Synapsis is pairing of homologous chromosomes.

Bivalents are seen.

Synaptinemal complex occurs between homologous chromosomes, that helps in precise pairing.

Pachytene:

Each chromosome splits longitudinally to form two chromatids attached at the centromere.

Bivalent changes into tetrad.

Crossing over, i.e., exchange of segments between non-sister chromatids occurs.

Crossing over occurs by the help of recombinase enzyme.

Diplotene:

Homologous chromosomes try to separate.

Chromosomes remain attached at regions where crossing over has occurred.

Chaisma is the regions where crossing over has occurred.

Chromosomes pull themselves apart from the centromere, as a result chaisma starts moving towards ends.

This is Terminalization, which starts in diplotene stage.

Diakinesis:

Terminalization completes forming ring-shaped chromosomes.

Nucleolus & nuclear membrane starts disappearing, spindle fiber formation starts.

Metaphase I:

Nucleolus & nuclear membrane has disappeared, spindle fiber formation is completed.

Chromosomes align on equatorial plate.

Anaphase I:

Homologous chromosomes separate due to contraction of spindle fibers, 

Terminal chaisma opens up & the chromosomes start moving towards poles.

Telophase I:

Chromosomes reach poles and uncoiling starts.

Nucleolus & nuclear membrane reappear, spindle fibers disappear.

Two nuclei one at each pole are formed.

Meiosis II – equational division:

Prophase II, Metaphase II, Anaphase II, Telophase II.

Meiosis II is same as Mitosis.

4 daughters cells each having haploid number of chromosomes are produced.

Also watch:Cell Cycle, Chromosomes.

Also read:

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