Posts Tagged ‘ reproduction ’

Introduction to Animal Behaviour Towards Sex

Introduction

It is believed that originally, species reproduced by asexual reproduction. This is where species are able to reproduce through mitosis individually, this means the descendants of the individuals are essentially clones, the only way which variation can occur is through mutations. Asexual reproduction allows for rapid population growth in stable environments (where adaptation through natural selection is not required). Examples of asexual reproducers are many bacteria, plants and fungi.

Sexual reproduction is the converse of this, requiring the gametes of two individuals to fuse together to form the next generation. Because of this, the life cycle of sexually reproductive individuals is typically divided into two phases; a diploid (2n) and haploid phase (n). Gamete production occurs by meiosis (which may introduce variation) where 2n -> n, the fusion of gametes (which also introduces variation) is the reverse, n -> 2n. With sexual reproduction a lot of variation arises each generation, which allows adaptation in changing environments.

The ‘Cost of Sex’

The cost of sex, also known as the cost of producing males is an equation that shows how parthenogenetic individuals (those who produce fertile female eggs asexually) are essentially twice as effective when compared to sexual reproduction. This means asexual individuals are able to quickly reproduce and populate an area, however they lack the variation introduced by sexual reproduction.

Imagine a population that consists of N sexual males and N sexual females (The total population would therefore be 2N). Each sexual female (N) can produce an amount of eggs, K. These eggs have a probability of surviving, S. So in the next generation there will be KSN sexual individuals, this is the number of females, the eggs they produce and the survival of those eggs.

Assuming that within this species there are also parthenogenetic individuals that produce asexually, n, which again produce K eggs with a survivability of S, the next generation of parthenogenetic individuals would consist of KSn. That is the total number of parthenogenetic individuals (n), the eggs they produce (K) and the survival rate of those eggs (S).

To determine the increase in proportion due to parthenogenetic individuals, we must find their proportion within the initial generation and the second generation. We will then be able to see how parthenogenesis compares.

The proportion of parthenogenetic individuals in the first generation was n/(n + 2N), this is the number of parthenogenetic individual divided by the total number of individuals (2N being the number if sexual males and females.)

In the next generation the ration will depend on the number of surviving eggs, which will be:

KSn/(KSn + KSN), this is the number of surviving parthenogenetic eggs, divided by the total number of eggs laid. Because the KS term appears on both the top and bottom, it can be cancelled out to give: n/(n + N)

If we assume that the parthenogenetic form arises as a mutant, we can say that n is very low when compared N. This is because the mutant(s) numbers are so small when compared to the rest of the species population. Because of this relationship we can assume that n + N is so close to the value of N alone, that n + N is roughly equal to N. We can say the same about n + 2N, this is roughly equal to 2N.

By making the above assumptions, the initial proportion on parthenogenetic individuals in the first generation is: n/2N

With the proportion increasing to: n/N in the second generation.

This shows that the proportion of parthenogenetic individuals doubles in one generation, meaning that asexual reproduction has a two-fold advantage over sexual reproduction – this is known as the ‘Cost of Sex’ or the ‘Cost of Producing Males’.

Gamete Production and Parental Investment

Species may exhibit variation in the type of gamete that they produce; for example humans produce two very different types of gametes – the egg which is slow and large compared to sperm which are small, motive and numerous.

Isogamy is believed to have been the first step along the path of sexual reproduction. Isogamy is when both sexes produce similar gametes, making them undistinguishable from one another. Organisms such as algae, fungi and yeast form isogametes.

In contrast to isogamy is anisogamy; this is the production of dissimilar gametes that may differ in size or motility. Both gametes may be motile or neither, however they will always be distinguishable from one another. The anisogamy observed in humans is known as oogamy.

Oogamy is a specialised form of anisogamy, where the female produces significantly larger egg cells, compared to the smaller, more motile spermatozoa. Both gametes are highly specialised towards their role, with the egg containing all the materials required for zygote growth and the sperm containing little more than the male genetic contribution. This does however allow for the sperm to be highly motile and travel the necessary distances required to fertilise the barely motile egg.

Because of this, we often see greater amounts of parental investment from the females of species as they put in nearly all the energy of producing the offspring. Parental investment is defined as, any investment by the parent to an individual offspring that increases the offspring’s chance of surviving (and reproductive success) at the cost of the parent’s ability to invest in other offspring.

Robert Trivers’ theory of parental investment predicts that the sex making the largest investment in lactation, nurturing and protecting offspring will be more discriminating in mating and that the sex that invests less in offspring will compete for access to the higher investing sex. Sex differences in parental effort are important in determining the strength of sexual selection. This is why in many species, the female will be particularly choosy when looking for a male to mate with, as she will be examining the males to see which one will provide the best genes to ensure her offspring’s reproductive success is maximised.

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Fertilisation

Below is the entire article on fertilisation, to see more articles like this, in full for free please visit our main site – www.jameswatts.co.uk ! Thank you !

Introduction

Fertilisation is an internal process in mammals, the gamete cells however are not fully mature when they leave the gonad (either testicle or ovary) and so continue a process of maturation right up to actual fertilisation, the ovum matures fully when it undergoes its second meiotic division, the process for sperm is as follows:

  • Sperm leaving the Sertoli cell are non-motile and their DNA (located in the ‘head’ of the sperm) is not condensed, sperm are not fertile in this state.
  • It normally takes 8-15 days for sperm to mature as they pass through the epididymis
  • Over this period, certain changes occur in the membrane and nucleus of the sperm. These changes are dependent on androgens.
  • The membranes of the sperm also develop zona pellucida constituent receptors (ZP3 protein) which is important for fertilisation

Ejaculation

Upon ejaculation sperm are deposited either in the anterior vagina or directly into the uterus. Despite billions of sperm being deposited only a few (100-1,000) sperm are considered competent (able to reach the site of fertilisation – the infundibulum of the oviduct, around 8-10 hours after ejaculation). The majority of these sperm pass into the peritoneum.

Up to 95% of sperm are expelled out of the vagina to be destroyed by macrophages. Oestradiol increases uterine activity to help passage sperm through the cervix and along the uterus. Only a small amount of sperm makes it to the isthmus, which acts in some species as a reservoir for the sperm for 24-40 hours after coitus. The sperm reach the isthmus by combination of the uterine activity and their own motility, taking around 2-7 hours. Abnormal sperm are prevented from passing any further up the female reproductive tract.

Survival times for the gametes in the female reproductive tract:

Ionic constituents such as citric acid in the isthmus inhibit sperm. This makes the sperm less motile. However at ovulation waves of sperm are periodically released into the ampulla, this is thought to be under the influence of hormonal control. At this point sperm become hyperactivated; they show exaggerated movement as they move to meet the egg influenced by a possible chemoattractant.

The fimbria (finger like projections at the end of the fallopian tube) help to move the ovum down the oviduct. Exogenous steroids (such as prescribed drugs) can affect the passage of the oocyte that is the basis of the mechanisms for the morning after pill in humans and misalliance steroid treatment in bitches.

Sperm Capacitation

Capacitated spermatozoa are ones that have undergone changes in the female reproductive tract enabling them to fertilise the ovum, this occurs in the isthmus. This process is reversible and no morphological changes occur. These changes can also be induced by simple dilation in a solution.

Capacitation occurs when there are alterations made to the plasma membrane. These include changes in the charge and the removal of cholesterol that decreases the cholesterol: phospholipids ratio.

Capacitation is responsible for the hyperactivated motility pattern, which leads to the wider and stronger beats of the tail to enhance motility.

The Acrosome Reaction

The sperm must penetrate through two layers of the ovum to fertilise it, these include the cumulus cells with their extracellular matrix and the zona pellucida. Sperm motility is important here to allow them to wriggle through the cumulus layer to reach the zona pellucida. The zona layer consists of 3 glycoproteins – ZP1, ZP2 and ZP3. ZP1 is mainly structural but ZP3 is a Ligand for the attachment of sperm and is species specific. Sperm develop a receptor for ZP3 as they mature in the male seminiferous tubules. The attachment of the sperm ZP3 receptor to the zona Ligand is responsible for the triggering of the acrosome reaction (in capacitated sperm). It is possible for non-capacitated sperm to attach but the acrosome reaction will not be induced.

Stimulation of the acrosome reaction requires an increase in intracellular Ca2+ that is induced by an ionophore – promoting rapid transport of Ca across the plasma membrane into the cell. The acrosome of the sperm cell swells and the membrane fuses with the over-lying plasma membrane. Vesicles are formed, which is followed by the removal of the outer membrane. Intracellular Ca and cyclic AMP levels increase.

After the acrosome reaction, binding of ZP2 receptors on the now exposed inner acrosome layer is essential to hold the oocyte and sperm together. The sperm is then able to work its way through the zona layer, with the aid of a digestive enzyme acrosin as well as its motility.

Summary:

  • Sperm reaches oocyte and releases hyaluronidase to digest hyaluronic acid rich cumulus cells
  • The enzyme acrosin is able to digest zona layers and membranes of the oocyte
  • Sperm cell membrane fuses with the egg cell membrane
  • Contents of the acrosome head are released into the egg
  • ZP3 ligand on the ovum binds to ZP3 receptor on the sperm
  • Binding of the ZP3 components releases further enzymes which allow the sperm to fuse with the egg

Sperm and Egg Fusion

Once sperm have made it through the zona layers and into the peri-vitalline space, the sperm head aligns away from the oocyte DNA to avoid complications arising. Sperm movement ceases and microvilli on the surface of the ovum interact with the sperm. This results in a change in electrical charge on the vitalline membrane resulting in hyperpolarisation.

Zygote Activity

The next steps of fertilisation ensure a diploid nature of the forming embryo and the prevention of polyspermy or meiosis.

Immediately after sperm and egg fusion intracellular Ca levels rise dramatically. This causes cortical granules to release their contents into the peri-vitalline space that disrupts the ZP receptors and prevents further binding by any other sperm. The increased Ca also activates secondary oocyte meiotic division.

Sperm head proteins decondense and a few hours after fusion, membranes form around each set of gamete haploid DNA to form two pronuclei. The pronuclei approach each other, the nuclear envelopes disappear and the two chromosome sets aggregate in prophase – this completes the process of fertilisation as the zygote can now begin mitotic division.

The majority of zygote cytoplasm comes from the oocyte and so even after vesicle membrane breakdown oocyte DNA dominates. Successful fertilisation requires the correct formation of proteins from the oocyte, most of which would have formed when the oocyte was still in the follicle – correct follicular growth is therefore important for successful fertilisation.

Mitosis of the zygote continues – cell cleavage results in the formation of blastomeres that are large cells. When the zygote is 8-cells large, the embryonic genome becomes active and it begins to synthesise its own ribosomal RNA. It is believed that cell differentiation occurs at the 8 cell stage as well, because separation of the cells at the 4 cell stage will result in 4 identical offspring, however separation at the 8 cell stage only results in a maximum of 5 identical offspring.

The zygote arrives in the uterus in the morulla or blastocyst stage still in the zona.

Oogenesis

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Introduction

Oogenesis is the female version of gametogenesis and is therefore the female equivalent of spermatogenesis. This process follows the immature, primordial ova right through to its maturation as a fertile ovum (egg).

Two processes which are important in cell division and therefore the creation of gametes (gametogenesis) are meiosis and mitosis, a quick recap on those process are shown below:

  • Mitosis – Typical cell division where the diploid (2n) chromosome number is kept. Mitosis results in the production of identical cells.
  • Meiosis – This type of cell division is usually associated with the production of gametes, it involves a reduction in the diploid (2n) chromosome count to a haploid (1n) chromosome count. Due to the occurrence of homologous recombination during crossover of genes, non-identical daughter cells are produced. Fertilisation sees two haploid cells (1n) fuse, which results in the restoration of the chromosome number to 2n.

Primordial Germ Cells

During embryonic life, primordial germ cells (the early stage sperm or ova) originate in the yolk sac endoderm where they migrate to the gonadal ridges (ventral to the lateral somites). The next step in their development depends on whether the embryo is destined to be male or female, whether the gonads are destined to be testes or ovaries:

  • Testes – Primordial germ cells migrate to the medulla of the gonadal ridge and become surrounded by mesenchymal cells to form primitive sex cords (seminiferous tubule precursors)
  • Ovaries – Primordial germ cells migrate to the cortex of the gonadal ridge. The germs cells undergo mitotic division to increase their number prior to puberty.

Stages of Oogenesis

The primordial germ cells differentiate into oogonia (s. oogonium), where by different processes they develop into oocytes. These oocytes enter interphase, undergoing meiosis until prophase 1, it is at this point all meiosis is halted, development will continue at fertilisation. All ova cells typically reach this stage before birth.

  • Oogonia (2n) undergo mitosis (oocytogenesis) forming primary oocytes
  • Primary oocytes (2n) undergo meiosis 1 (ootidogenesis) forming secondary oocytes, the primary oocytes are halted in prophase 1 of meiosis until ovulation
  • Secondary oocytes (1n) undergo meiosis 2 (ootidogenesis), remaining in metaphase 2 until fertilised

Development of Follicles

Mesenchymal cells begin to surround the oocytes, which forms the primordial follicles. These surrounding cells eventually become cuboidal to form the granulosa cells. The follicle grows as the layers of granulosa cells increases; growth of the oocyte also contributes.

Gonadotrophins such as LH and FSH stimulate further follicular growth causing a cohort of follicles to emerge as a follicular wave (from which one will become dominant and be ovulated).  Fluid spaces develop in the granulosa cell mass (antrum formation) making the structure an antral follicle. The oocyte within the follicle remains attached to one edge of the internal follicle wall surrounded by cells of the cumulus (cumulus oophorus).

At regular intervals, from the cohort of follicles that initially emerge in the follicular waves some are selected to develop – they develop larger antral spaces. From the smaller group of selected larger follicles, typically only one becomes dominant – the others undergo atresia (the process of degeneration of follicles that are not ovulated in menstrual or oestrous cycle).

The oocyte within the follicle is still at the primary oocyte stage – it is still halted at prophase 1 of meiosis. However under the influence of a gonadotrophin surge associated with the process of ovulation, the process of meiosis resumes within the oocyte. The oocyte undergoes a meiotic division to form two differently sized cells, a large secondary oocyte and the first polar body. It is at this point ovulation takes place, meiosis again halted (until fertilisation).

Upon fertilisation by a spermatozoon, meiosis resumes, the secondary oocyte undergoes a second meiotic division to again produce two differently sized cells, a large zygote (a diploid [2n] cell resulting from the fusion of two haploid [1n] cells) and a smaller second polar body. The secondary oocyte, after being ovulated, has only a short period in which it can be fertilised – resulting in the development of the embryo.

Female Reproductive Anatomy Questions

If you need to know about the female reproductive tract, specifically in domestic animals, then it may be worth your while taking a look at these questions. They are in .csv format meaning you can view them in excel, however if you have flashcard software such as mentalcase or gFlash+ then if you leave a comment below I shall send you the link to download them in a better format for your flashcard software!

Hope they help – 127 questions on the female from the ovary to the vestibule as well as including a summary of parturition times and lengths.

Here is the link: (Remember to right click and click Save Target As… if you want to open it in excel!)

http://dl.dropbox.com/u/2561295/Website/234/Questions/Female%20Reproductive%20Anatomy.csv

Luteolysis

Introduction

Luteolysis is the degradation of the corpus luteum (as opposed to luteinisation – the formation of the corpus luteum). Luteolysis occurs in the absence of pregnancy, at the end of the luteal phase. The process of luteolysis is initiated by oxytocin (secreted by the corpus luteum) and prostaglandin F2a in domestic animals.

Mechanism

Progesterone is produced by the corpus luteum, which inhibits the hypothalamus (the hypothalamus secretes GnRH, therefore progesterone inhibits GnRH secretion). The corpus luteum also secretes oxytocin.

Initially the oxytocin appears to have no effect, however after a short period of time (e.g. 12-15 days in the cow) oxytocin receptors begin to form. When these oxytocin receptors are stimulated by the oxytocin secreted by the corpus luteum, prostaglandin F2a synthesis and secretion by the endometrium is stimulated.

Prostaglandin inhibits the production of progesterone (which is inhibiting the GnRH secretion and thus preventing the emergence of new dominant follicles). If progesterone production is inhibited then the oestrous cycle is able to begin again.

Prostaglandin also stimulates further oxytocin release, stimulating more oxytocin receptors that cause further prostaglandin F2a release. This is known as a positive cascade system and is used to quickly progress a biological situation, here the situation would be the prevention of inhibition of progesterone (which is inhibiting GnRH secretion).

The reduction of plasma progesterone concentration means follicular growth can now continue and dominant follicles can now emerge. In pregnancy, there is no corpus luteum formation (luteinisation) so there is no luteolysis – therefore progesterone levels remain high.

Summary

  1. Corpus luteum produces progesterone and oxytocin – progesterone is inhibiting GnRH secretion
  2. Oxytocin receptors form
  3. Stimulated receptors cause prostaglandin F2a by endometrium
  4. Prostaglandin inhibits the secretion of progesterone and stimulates further oxytocin release
  5. Positive cascade system rapidly increases plasma prostaglandin concentration
  6. Progesterone levels are low again and GnRH secretion resumes
  7. Follicular development begins again, ready to repeat the oestrous cycle

Spermatogenesis

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Introduction

Spermatogenesis is the biological process whereby spermatogonia (the germ cell) develop into spermatozoa (the mature sperm cells). This process takes place in the seminiferous tubules of the testes; this is the starting point for spermatogenesis. Stem cells adjacent to the inner tubule wall divide, beginning at the walls and proceeding into the innermost part, or lumen producing immature sperm. Maturation occurs in the epididymis where sperm develop a tail and become motile.

Anatomy of the Testes

Seminiferous tubules comprise the majority of the structure of the testes. The remaining spaces between the tubules are occupied by interstitial tissue.

Interstitial Tissue

The interstitial tissue comprises mainly of blood vessels, lymph gaps, connective tissue and Leydig cells (specialised cells found in interstitial tissue adjacent to seminiferous tubules). Mast cells and macrophages are also present in small numbers.

Leydig Cells – These cells have an abundance of smooth endoplasmic reticulum and no rough endoplasmic reticulum, along with large amounts of mitochondria, lipid droplets and centrioles. They also have a prominent Golgi complex. Another cell specific feature is the receptors they have on their cell membrane that are highly specific to luteinising hormone (LH) – This differentiates them from other testicular cells, as they are the only cells to have these receptors.

Follicle-stimulating hormone (FSH) increases the response of Leydig cells by increasing the number of LH receptors expressed on their surface. The LH receptors when stimulated secrete steroidal hormones such as testosterone. Testosterone has a key role in the development of spermatozoa (spermatogenesis).

Seminiferous Tubules

Typical seminiferous tubules include the Sertoli cells and germ cells. The epithelium of these tubules is known as the germinal epithelium. The seminiferous tubules have a fluid filled lumen; mature spermatids are released into this lumen as fully mature spermatozoa. Myoid cells surround the basement membrane of seminiferous tubules; they are contractile in nature and their contractions move sperm along the seminiferous tubules.

Sertoli Cells

Sertoli cells have a main function in the nurturing of spermatozoa through their early stages of development from germ cells right up to their mature spermatid form (before being released into the seminiferous tubules to become spermatozoa). Sertoli cells therefore have a prime role in the co-ordinating of spermatogenesis – without Sertoli cells, spermatogenesis cannot take place.

Near the base of the cells in their lateral walls, tight junctions join Sertoli cells to one another. The formation of tight junctions means that inter-cellular diffusion of material is prevented. The tight junctions form a complete barrier that divides the tubule into a basal compartment and an adluminal compartment. Different types of germ cells occupy the different compartments. This barrier forms a blood-testes barrier, which isolates spermatocytes from the rest of the body, allowing for the environmental conditions required for spermatogenesis.

An important feature of the blood-testes barrier is that it prevents immune cells from reaching the haploid cells produced during spermatogenesis. This is important because the haploid cells are not recognisable as ‘self’ cells, meaning if the immune cells could reach them, they would destroy them. If damage were to occur to the tight junctions forming the blood-testes barrier, immune cells would be able to come into contact with the germ cells triggering an immune response and the production of antibodies causing the sperm cells to become non-functional – resulting in infertility of the male. Sertoli cells are also unable to proliferate; the body is unable to replace any lost Sertoli cells.

Sertoli cells have cell-membrane receptors specific for FSH, which when stimulated increases production of cyclic AMP

They are also able to convert cholesterol to pregnenolone, which is then converted to testosterone. They also produce specific proteins such as androgen binding protein under the influence of FSH and testosterone.

Cryptorchidism

Below is only the introduction to this article on cryptorchidism, if you are interested and this is what you were looking for, then head over to our website, where you can download this article and many more for free! If you don’t want to download them, then it is possible for you to view them online in your browser!

Also remember to check out the new questions being added all the time, you can see which articles have questions by searching the index, where you will see a link next to the article like this [Questions]

Introduction

Cryptorchidism is a disorder where either one or both testes fail to descend and are therefore absent from the scrotum.  This usually occurs during foetal development when the testes begin their movement or descent from an abdominal position through the inguinal canal into the scrotum. Because the testes have failed to descend and therefore remain within the body, the temperature is too hot for sperm production to occur, rendering the male infertile.

There are however varying levels of cryptorchidism:

• Undescended testicles may later fully descend (usually within 1 year) leaving the male without fertility problems

• Testicles which have not fully descended but have partially reached the scrotum may be able to produce some sperm

• Only on testicle may not descend, but as the other will have fully descended the male will be fertile

• If both testicles fail to descend (bilaterally cryptorchid testes) then the male is infertile

Only sperm production is affected however (due to the high body temperature) which means that the natural hormone production of the testes are unaffected, the male will still behave normally therefore and express normal sexual behaviour.

The possible outcomes of testes failure to descend:

• Testis could be found anywhere along the “path of descent” from high in the posterior (retroperitoneal) abdomen, just below the kidney, to the inguinal ring

• Testis could be found in the inguinal canal

• Testis could be ectopic, that is, found to have “wandered” from that path, usually outside the inguinal canal and sometimes even under the skin of the thigh, the perineum, the opposite scrotum, and femoral canal

• Testis could be undeveloped (hypoplastic) or severely abnormal (dysgenetic);

• Testis could have vanished – May therefore be anorchid or monorchid (Not formed)