#diplotene

[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]

In Meiosis divisions, chromosomes appear a single in Leptotene followed by convergence and adhesion of identical chromosomes in Zygotene, then duplicated in Pachytene followed by separation f chromosomes to chromatids in Diplotene, then formation of the spindle occurs in Diakinesis. Then, bilateral shrinking chromosomes are arranged in the center of spindle fibers in Metaphase 1. After that, separation of identical chromosomes from each other occurs to the opposite site in Anaphase 1. Next, cytoplasm divided and two daughter cells are formed in Telophase 1. Then, formation new regular bilateral chromosomes occurs at the equator spindle in In Metaphase 2. Next, breakup of chromosomes to two groups and chromatids separate occurs in Anaphase 2. After that, 4 nuclei formation occurs with a single chromosomal haploid group in Telophase 2 #geneticteacher

[sciencesolutions]

[whats-in-a-sentence]

Towards the end of pachytene, chromosomes have condensed enough to be seen in the microscope as distinguishable threads (see Figure 2.5). (...) During normal meiosis, the chromosomes of a diploid germ cell undergo DNA replication followed by two rounds of division (meiosis I and meiosis II), producing four haploid cells (see Figure 2.5). (...) Diploid interspecies hybrids occur naturally, but they are frequently sterile because their chromosomes cannot pair properly during prophase I of meiosis (see Figure 2.5).

"Plant Physiology and Development" int'l 6e - Taiz, L., Zeiger, E., Møller, I.M., Murphy, A.

[ma-douce-souffrance]

Zygotene pachytene diakinesis diplotene ajhsjahfljaflsgflkhalkfagfhkagfskhagfkhagakhs

is this some chemistry stuff?

[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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[biologyweeps]

hey so i'm in 3rd semester of biology and we've heard repeadetly that eggs are almost fully formed at the woman's birth (mid-end meiosis 2) but sperms are always contineously generated anew. so sperms are affected by stem cell age. then why is the mother's age always pointed to as cause for i.e. trisomy 21? wouldn't the father's age have a much greater impact on genetic defects caused by bad cell division???

Well it’s pointed out because that’s what the evidence is looking like and the reason for it is this:

The oocytes aren’t really fully formed. By the time of birth, the number of oocytes is already fixed and you can’t get more, but is then stopped during prophase I until sexual maturation is reached and then only the oocyte that actually gets to ovulate does go all the way through meiosis. Well technically it goes to metaphase II and the rest only happens after fertilization but that’s not the important bit here. The important bit is prophase I, in which the vast majority of eggs is stuck.

Specifically, they get stuck in the phase of prophase I called the diplotene. The important part here is that normally in this phase the chromosome pairs get divided up, except in spots where crossing over happens. There they get stuck together. And that’s the key here. Because if you got two chromosomes that are already stuck together, there’s a certain chance that during the next step, they might separate properly, so instead of pulling one whole chromosome onto each side of the cell and get on dividing, it’s possible that one side may get a whole chromosome and one chromatide of the other. And then you suddenly got 1.5 chromosomes and if things in the further meiosis go wrong - or right depending on how you wanna look at this - the result can be that you have two chromosome 21 already sitting in the cell before any sperm get involve, with the known result of trisomy 21.

So the female gametogensis in humans runs a higher risk of ‘tugging’ an extra chromatide somewhere because they spent so much time in prophase I. They can spent the entire time to menopause in prophase I if the oocyte never gets to mature through for ovulation. 

[shimashimashippo]

on meiosis: oogenesis & spermatogenesis

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

(disclaimer: 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 and diagrams.)

meiosis is often taught to be a matter of one diploid cell becoming four haploid cells to create our sex cells ー simple, right? well, while that may be the case in spermatogenesis (the production of sperm) (although, we’d be leaving out the multiple round of mitosis necessary to even initiate meiosis), it is not so much in oogenesis (the production of eggs) which oftentimes actually produces only three cells ー two of which only serve to help the math along and make the one egg haploid but are otherwise technically useless. with that said...

let’s start with oogenesis [1][3*][4], shall we? 

during gestation, you start out with primordial germ cells (PGC ー think “stem cells,” not “germ = bacteria / gross stuff” because in actuality “germ cells = sex cells”) which migrate to the ovaries where they divide to form oogonia, self-renewing stem cells. the oogonia then continue dividing for some time (and make more of themselves, hence “self-renewing”). around the seventh month of gestation, several oogonia die off. as for the remaining, they prepare to go through meiosis and become what are called primary oocytes ー the “initial” diploid cell that splits twice to (supposedly) create four haploid cells.

the primary oocyte enters prophase I where it has to go through five phases:

leptotene ー homologous chromosomes start associating and then condensing

zygotene ー synapsis occurs between the homologs (they’re sticking really close together now)

pachytene ー  crossover & recombination

diplotene ー (also called the dictyate state) your oocytes hang out here until puberty starts and you start releasing eggs (even then, some die in the process); so the chromosomes decondense while remaining attached at chiasmata (sites of crossover) to allow for transcription to sustain the cell in the meanwhile.  in mice, the genes ZP1, ZP2 and ZP3 are transcribed to produce the glycoprotein layer called the zona pellucida (ZP) that surrounds the oocyte and in part serves as a fertilization barrier across species.

diakinesis ー chromosomes recondense and prepare for metaphase I

it then continues through and finishes up meiosis I to divide asymmetrically and produce two cells ー a secondary oocyte and a polar body. what do i mean by “divide asymmetrically”? the genetic material is divided evenly between the secondary oocyte and polar body but the machinery (cytoplasm / cytosol, ribosomes, lysosomes, golgi, etc.) are not! the secondary oocyte gets most of the machinery while the polar body gets very little which is why i don’t particularly think the polar body can sustain itself very well to go through another division itself. the secondary oocyte is obviously fine for going through meiosis II, though, because that’s exactly what it does!

the oocyte is again arrested / halted in metaphase II because here, it has two options:

get fertilized ー sperm binds with the egg to produce some conformational change that basically tells the egg to hurry up, get through meiosis II and spit out another polar body. once that’s done, sperm membrane then fuses with the oocyte membrane (called the “oolemma”) and deposits its genetic material. as the female and male pronuclei (two haploid nuclei) approach each other, they duplicate their genetic material and string them together on the spindle fibers for a round of mitosis; thus creating a two-cell embryo! (i believe the zygote is the single cell containing both pronuclei before mitosis. after mitosis, it becomes multicellular; so embryo.) [x]

not get fertilized ー you bleed (more on this later!)

*you may not actually have access to article #3 / i have to use my university’s library vpn. but even then all i took from it for this post is the first few sentences to this section.

now, for a bit on spermatogenesis, which is perhaps a bit more complicated [2]! in the testes are these coiled seminiferous tubules, in which lie our PGCs gathered around sertoli cells for nourishment and protection [x].

first, prepare yourself for several rounds of mitosis followed by incomplete cytokinesis (cleavage furrow forms, but the cells don’t entirely split ー they just hang out connected in a chain) as described below!

once the PGCs reach the testes, the divide to form type A1 cells, which are smaller than the PGCs and lie near the walls of the tubule

the type A1 cells divide to produce paler type A2 cells

type A2 begets type A3

type A3 begets type A4 it is believed that the type A cells are capable of self renewal (so, for example, type A1 can divide to produce more type A1 or type A2); thus, type A4 now has three options: self-renewal, apoptosis (cell death), or ...

type A4 can differentiate into intermediate spermatogonia and commit to becoming spermatozoa (the fancy word for mature motile sperm)

the intermediate spermatogonia divide once to become type B cells

finally, type B cells divide once to become primary spermatocytes ∴ PGC → A1 ⇌ A2 ⇌ A3 ⇌ A4 → intermediate → B → primary

now we can start talking about meiosis, which is fortunately not as complicated as in oogenesis! in fact, it’s more like your textbook explanation of meiosis. 

each primary spermatogonium divides to become two secondary spermatogonia (no polar bodies!). each secondary spermatogonia divides to produce two haploid spermatids. again, every round of division is still followed by incomplete cytokinesis which allows molecules and whatnot to pass between all of them freely so that they can all mature at the same time / pace. this also allows the spermatids to be functionally diploid while being actually haploid. [x]

during the progression from type A1 to spermatid, the cells migrate towards the lumen (google defines this as the “inside space” but here think “center” of the tube).

but we’re not quite done. our spermatids are still connected ー how do they mature and split apart? how do they become able to move and migrate toward the egg? how do they get ready to bind to (and eventually fuse with) the egg? let’s talk a bit about spermiogenesis [5] ー the “differentiation of the sperm cell.” we must consider three things: the nucleus, the acrosome and the axoneme.

the nucleus begins to change shape and condense itself into the “dense, species-specific head shape that is important for motility.” similarly, the genetic material is also condensed into chromatin fibers. 

from the golgi bodies buds little granules that will come together to form a vesicle we will call the acrosome that contains enzymes important for fertilization (i.e. binding to and burrowing through the zona pellucida surrounding the MII oocyte). the acrosome is then attached to cover much of the nuclear surface.

the axoneme is basically its tail / flagellum which allows it to move around and hopefully towards the egg. using the centrosome as a base, the axoneme forms and acquires “outer dense fibers, the fibrous sheath and the mitochondrial sheath.” the outer dense fibers and fibrous sheath allow it some rigidity as the sperm makes it way up the tortuous path in search of the egg. meanwhile the mitochondrial sheath supplies it the energy needed.

finally, in spermiation [6] the mature spermatid is released ー “pushed” out of its cytoplasm / cytosol which is left behind to condense and be ingested by the sertoli cell ー into the lumen to become what is now called a spermatozoon.

so there you have it! i’ll be discussing menstruation & ovulation next. 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

[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

Go to

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].

Go to

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.

[essayeditorblr-blog]

Different essay formats

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Different essay formats

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[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

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