How are germ cells not reduced in number?

How are germ cells not reduced in number?

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If germ cells produce haploid daughter cells by meiosis and are thereby "consumed" (where there was a germ cell there are then 4 daughter cells), where do the germ cells come from? I asked my biology teacher if they undergo mitosis prior to meiosis, but she said they don't and proceeded to give an unclear answer. Is this true? If so, are they regenerated from somatic cells elsewhere in the body?

My question basically is - if the germ cells of, say, the testes are dividing by meiosis to produce sperm, where are the germ cells coming from so that the testes don't shrink and ultimately disappear as they're converted completely into sperm?

In case of gametogenesis (let us talk about spermatogenesis) gametes are formed from meiotic division of Primary spermatocytes.

In Primates Primary spermatocytes are cells that that are formed from mitotic division of B spermatogonia (which is another class of germ cells) which inturn are formed from mitosis of Ap spermatogonia which arise from mitotic division of Ad spermatogonia. Ad spermatogonia are inturn formed from Primordial germ cells (see below for details).

Ad spermatogonia are dark A type spermatogonia, reserve stem cells which occasionally divde to renew itself and Ap spermatogonia are pale A type spermatogonia, renewing stem cells.

Why the testis doesn't run out of germ cells? (adaptation of your key question)

The reserved Ad spermatogonia and renewal of both Ad and Ap spermatogonia are responsible for the continuous cycles of spermatogenesis.

This process starts at puberty and usually continues uninterrupted until death, although a slight decrease can be discerned in the quantity of produced sperm with increase in age. (wikipedia)

The process of spermatogenesis in human:

In non-primates like mice it is little different, the following diagram should explain it:


  • Germ cells are cells that give rise to gametes ( present at any level of gametogenesis).
  • Primordial germ cells are embryonic cells that originate from a different location (outside the gonads) and migrate into the gonads during the course of embryonic development to divide into germ cells.
  • In females, oogenesis also involve production of germ cells (cells of primary follicles) from PGCs through mitosis but the primary follicles produced is fixed, doesn't increase after birth so at a definite age of 40-45 gametogenesis stops.

Further reading:

  • Stem Cells in Reproductive Medicine by Carlos Simón, Antonio Pellicer, Renee Reijo Pera
  • A paper

"How are germ cells not reduced in number?"

It does happen. Germ cells do eventually run out. It is called menopause in women. And age related infertility in men.

As for your question of where do germ cell come from? Much like were do muscles cells come from?, you have to be specific. Germ cells comes from the gonads (ovaries and testis) would be a simple answer.


They are coming from Spermatogonial stem cells (SSCs), cells that for the most part are immortal, and can replicate endlessly (well ~60 years anyway).

Germ cell

A germ cell is any biological cell that gives rise to the gametes of an organism that reproduces sexually. In many animals, the germ cells originate in the primitive streak and migrate via the gut of an embryo to the developing gonads. There, they undergo meiosis, followed by cellular differentiation into mature gametes, either eggs or sperm. Unlike animals, plants do not have germ cells designated in early development. Instead, germ cells can arise from somatic cells in the adult, such as the floral meristem of flowering plants. [1] [2] [3]


Variation in recombination rates in humans and other diploid organisms can be shaped by evolutionary and molecular processes [1], but these forces are only partially understood. High-resolution human recombination maps have been estimated using both parent–offspring transmission [2, 3] and patterns of linkage disequilibrium (LD) [4,5,6,7]. These have revealed localized regions with higher or lower recombination rates, known as recombination hotspots and coldspots, respectively [5]. Sequences analysis has shown that human recombination hotspots are associated with a number of sequence features such as PRDM9 binding motifs [8], CpG islands, and GC-rich repeats [4, 5, 9], and that recombination coldspots are associated with repetitive elements, transcribed regions, and telomeres [5, 6].

Outside recombination hotspots, differences in epigenomic signatures are associated with differences in recombination rate [10, 11]. In particular, the level of DNA methylation, primarily established at prophase I when recombination occurs [12], is reported to be positively correlated with recombination rate [11]. A causal effect of DNA methylation on recombination rate was established using a methylation-deficient strain of Arabidopsis, which showed reduction of recombination rate in euchromatic regions [13, 14].

Germ Cells, Fertilization and Sex

Germ cell sex determination may depend on cell signals and genetic constitution.
In the mouse, the precursors of the germ cells (PGCs) are induced in the proximal epiblast by signals from the extra-embryonic ectoderm.
During gastrulation, these move to the posterior, above the primitive streak to form a cluster in which the centrally located cells become specified.
Once specificed, the primordial germ cells migrate to the gonads,
In the mouse embryo, pre-germ cells enter the genital ridge (where the gonads form) and continue dividing.
In the female, cells enter meiotic prophase and arrest until the mouse matures.
In the male, the cells continue to divide but eventually arrest in the G1 phase.
After the mice are born, the cells start dividing again and enter meiosis with maturity.
Mouse germ cells that enter meiosis before birth become eggs and those that enter later become sperm.
Mouse germ cells that fail to enter the genital ridge, start to develop as oocytes (in both males and females) but later development is abnormal.
Differentiation of the germ cells depends upon a reduction in the number of chromosomes (meiosis) but oogenesis and spermatogenesis have different approaches.
Note: In the formation of oocytes, the timing of meiosis (and the formation of polar bodies) varies in different organisms, and is completed in some organisms only after fertilization.
In humans, the number of oocytes decline with age via apoptosis (6-7 million in the early fetus, 400,000 oocytes at puberty): 400 to 500 are released throughout a lifetime.
Both maternal and paternal genomes required for normal mouse development.
Imprinting of genes, such as IGF-2 in mouse, are at least partially responsible for this requirement.

Fertilization involves cell-surface interactions between egg and sperm.
The sperm has to pass several barriers to enter the egg.
For fertilization of mammalian eggs, the sperm first passes through a layer of cumulus cell embedded in hyaluronic acid aided by the hyaluronidase actvity on its surface.
The 2nd layer is the zona pellucida, a layer of glycoproteins.
The acrosomal reaction (release of enzymes in the sperm head) is mediated by interaction of the ZP3 species-specific receptor and adhesion molecules in the sperm head.
The acrosome releases acrosin (a protease) and an acetylglucosaminidase (which degrades glycoprotein side-chains).
The sperm surface which contains proteins (i.e. fertilin) that can bind the egg's surface are exposed during the acrosomal reaction.
Fertilin binds an intergrin-like receptor of the egg plama membrane to initiate sperm-egg fusion.
In some invertebrates (i.e. sea urchins), an actin filament-driven acrosomal projection allows the sperm and egg to meet through a coat of jelly.
Changes in the egg membrane at fertilization to block polyspermy include, in the sea urchin, depolarization and the release of cortical granules.
Only one sperm may enter an egg.
To prevent polyspermy, enzymes that prevent other sperm from binding to the zona pellucida are released.

At fertilization a number of events occur to activate development (such as increase in protein synthesis, structural changes [cortical rotation]).
Main event is the completion of meiosis, fusion of the nuclei to form a diploid zygotic genome and entry into mitosis.
A calcium wave initiated at fertilization results in egg activation.
The sharp increase in calcium initiates the cell cycle by acting upon proteins that control the cell cycle.
The Xenopus egg is kept in metaphase II by maturation-promoting factor (MPF) a complex including cyclin.
The calcium wave activates a kinase which results in the degradation of cyclin which allows the meiosis to finish & the nuclei to fuse.

Determination of Sexual Phenotype
The early male and female embryos are very similar and differentially develop in latter stages.
Even in some vertebrates, gender is not always chromosome dependent (i.e. temperature at which the alligator embryo develops determines gender and some fish can change sex depending on environment).
In mammals, sex-determining region on the Y chromosome (Sry), once known as the testes-determining factor encodes a transcription factor that specifies malesness.
Translocation of the Sry region to the X results in XX males and Sry alone injected into XX mouse eggs produce males.

Mammalian sexual phenotype is regulated by gonadal hormones
All mammals begin development as gender neutral, the presence of the Y chromosome induces testis development that produce hormones that switch the development of somatic tissues into the male pathway.
This means that the sex of only the gonads is genetically determined but the rest of the cells are neutral (whatever their chromosome complement is).
Their fate depends upon hormones.
The mesonephros (embryonic kidney) contribute to both male and female reproductive organs.

Wolffian & Mullerian ducts
On the sides of the mesonephros are the Wolffian ducts and Mullerian ducts that open into the cloaca.
In females (in the absence of the testes), the Mullerian ducts develop into the oviducts (Fallopian tubes) and the Wolffian ducts degenerate.
In males, the Wolffian duct becomes the vas deferens.
The genital region differentiates after gonad development with the action of the gonadal hormones.

In mammals, signals from the gonad control germ cell identity as either egg or sperm.

Drosophila sex determination

In Drosophila,
1) XY germ cells transplanted to a female enter the embryo and
2) XX germ cells transplanted into a testis both develop as non-functional sperm to demonstrate both cell autonomy and environmental signals.

Gynandromorphs are genetic mosaics in which one X is lost in half of the organism(ie. left XX is female and right XO is male).

The primary sex-determining signal is the number of X chromosomes.
The Sex-lethal (Sxl) protein acts as a stable binary genetic switch.
The presence of two X chromosomes results in the production of Sxl .
The presence of Sxl results in the proper splicing of the tra mRNA production of the transformer protein.
Downstream, male and female versions of the double sex gene product are made by sex-specific splicing of dsx mRNA.
Tra protein (plus Tra2) leads to the splicing of the female dsx mRNA.
The male dsx mRNA is the default product and is made in the absence of female signaling.

In C. elegans, the differences between the male and the hermaphrodite somatic sex determination are controlled by another binary switch mechanism.
The germ cell identity of C. elegans is passed upon timing in the hermaphrodite, as sperm is made initially (and stored) and eggs are made later.

Various strategies are used for dosage compensation of X-linked genes.
The imbalance of X linked genes between males and females must be corrected (dosage compensation).
Mammals achieve this by inactivating one of the two female X chromosomes after the blastocyst has been implanted in the uterine wall.
The inactive X can be seen in the nucleus as a Barr body.
Xist, is a genetic switch, which produces an RNA that interacts with the "X inactivation region" of the X chromosome.
In Drosophila, the opposite approach is used when Sxl is off, transcription from the single X chromosome is doubled (translation increases as well).

As a gene controlling coat colour in cats resides upon the X-chromosome, X-inactivation leads to very obvious mosaicism in heterozygous females.
Other mammalian females, including humans, are less obvious in their mosaic patterning due to X-inactivation.


The PGCs are formed distantly from their final destination, thus, they must migrate for a long distance to reach the GR. The precise mechanism that regulates the directional migration of PGCs towards the GR remains an open question [47]. The widely accepted hypothesis suggests that the PGCs are attracted by the factors that are emitted from the destination or by somatic cells along their migratory route. In vitro studies have demonstrated that the GR tissue from E10.5 embryos attracts PGCs migration [35]. Several genes have been implicated in the process of PGC migration, such as Sdf-1, Steel factor, Integrinβ1 [8, 15] and E-cadherin [14], and the inactivation of these genes results in aberrant PGC migration. In this study, a GR-deficient mouse model, Wt1 R394W/R394W , was used to study the roles of the GR in germ cell migration and development. We found that the migration of PGCs in GR-deficient embryos was normal, which was consistent with a previous study [33]. Stella-positive PGCs reached the mesenchyme under the coelomic epithelium at E10.5, and no ectopic PGCs were observed in GR-deficient embryos. However, the number of PGCs was dramatically reduced in GR-deficient at E11.5 and E12.5. Further study revealed that the decrease of PGC number was due to the reduced proliferation but not cell apoptosis.

Sdf1, Steel factor and Integrinβ1 have been reported to play important roles in regulating PGC migration [8, 15]. In this study, we found that the expression of these proteins was not restricted to GR somatic cells and the protein level was also not changed in Wt1 R394W/R394W embryos compared to control embryos. These results suggest that the signals that regulate PGC migration probably not only come from GR somatic cells, but the factors from hindgut, mesentery and the mesenchymal cells around GR also play important roles in this process. Given that PGCs begin to migrate at approximately E7.5, while the GR is not visible until approximately E9.5 in mice, the early stage of PGC migration is most likely regulated by somatic cells along the migrating pathway, not by signals from the GR. In this study, we found that the GR development was blocked in Wt1 R394W/R394W embryos due to Wt1 mutation. However, the coelomic epithelium was still maintained from E9.5 to E12.5. We could not exclude the possibility that the developmentally arrested coelomic epithelial cells still can secret some unknown factors which attract the PGC migration, and other functional GR is not essential for germ cell migration. We also found that most of the PGCs in control and Wt1 R394W/R394W embryos arrived at the mesenchyme near the coelomic epithelium at E10.5. However, at E11.5 and E12.5, all the germ cells in control embryos were colonized into the developing GR (Figure 3B, C), whereas, the germ cells in GR-deficient embryos were scattered widely under the coelomic epithelium instead (Figure 3E, F). These results suggest that GR somatic cells are important for the precise positioning of PGCs at the final step of migration.

During and after colonization into the GR, PGCs proliferate rapidly, and their number is increased dramatically from approximately 500 to 25,000 by E13.5 [48, 49]. After sex determination, most germ cells enter mitotic arrest [20, 21]. Whether the proliferation of germ cells is a cell autonomous process or regulated by GR somatic cells is unclear. In this study, we found that the proliferation of PGCs was dramatically reduced in Wt1 R394W/R394W embryos at E11.5 and E12.5 compared to control embryos, whereas, the germ cells in Wt1 R394W/R394W embryos were still mitotically active at E13.5 when all the germ cells stop proliferation in control embryos, indicating that the proliferation of germ cells is precisely regulated by GR somatic cells during the early stage of gonad development, and disruption of GR development results in aberrant germ cell proliferation. Our results were consistent with previous in vitro studies, which showed that soluble factors released by GR regulated the proliferation of PGCs using the medium conditioned by different embryonic tissues [35].

Zfx mutation results in small animal size and reduced germ cell number in male and female mice

The zinc-finger proteins ZFX and ZFY, encoded by genes on the mammalian X and Y chromosomes, have been speculated to function in sex differentiation, spermatogenesis, and Turner syndrome. We derived Zfx mutant mice by targeted mutagenesis. Mutant mice (both males and females) were smaller, less viable, and had fewer germ cells than wild-type mice, features also found in human females with an XO karyotype (Turner syndrome). Mutant XY animals were fully masculinized, with testes and male genitalia, and were fertile, but sperm counts were reduced by one half. Homozygous mutant XX animals were fully feminized, with ovaries and female genitalia, but showed a shortage of oocytes resulting in diminished fertility and shortened reproductive lifespan, as in premature ovarian failure in humans. The number of primordial germ cells was reduced in both XX and XY mutant animals at embryonic day 11.5, prior to gonadal sex differentiation. Zfx mutant animals exhibited a growth deficit evident at embryonic day 12.5, which persisted throughout postnatal life and was not complemented by the Zfy genes. These phenotypes provide the first direct evidence for a role of Zfx in growth and reproductive development.


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Find Out How the Gametogenesis Process Works

Gametes are cells specialized in sexual reproduction. They contain half of the maximum number of chromosomes of the species and unite with another gamete to give birth to a zygote with double of number of chromosomes of the gametic cells.

In humans, gametes are formed by meiosis male gametes are sperm cells and female gametes are egg cells.

Meiosis and Gametogenesis

More Bite-Sized Q&As Below

2. What type of cell division permits sexual reproduction? What is gametogenesis?

Meiosis is the type of cell division that allows sexual reproduction, since it reduces the number of chromosomes of the species to a half, making the combination of two gametes to form a new individual possible. (In some organisms, meiosis creates haploid gametophytes that by means of mitosis generate gametes. Even in this case, the function of meiosis is the same: to provide cells with half of the number of chromosomes of the species, with the separation of homologous.)

Gametogenesis is the name given to the process of gamete production.

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Gonads and Germ Cells

3. What is the name of the cells capable of making gametes? What is the ploidy of these gamete-forming cells?

The cells that form gametes are germ cells, as opposed to somatic cells. The ploidy (number of chromosomes) of germ cells is the same as somatic cells (only during the formation of gametes does meiosis occur, reducing the number of chromosomes to half).

4. What are gonads? What are the male and the female gonads in humans?

Gonads are the organs that produce gametes. They contain germ cells that undergo division and generate gametes. In males, the gonads are the testicles. In females, the gonads are the ovaries.


5. Indicating the name and respective ploidy of each cell involved, how can the formation of sperm cells from germ cells be described?

The formation of sperm cells, or spermatogenesis, begins with a germ cell called the spermatogonium (2n), which undergoes mitosis and gives birth to the spermatocyte I (2n). The spermatocyte I undergoes meiosis I and generates two spermatocyte II (n) cells, which then undergo meiosis II and produce four spermatids (n). Each spermatid undergoes a maturation process called spermiogenesis and four sperm cells are produced.

6. What is the difference between spermatogonium and spermatocyte I cells?

The male germ cells are spermatogonia (diploid cells, 2n),which are located in the testicles. They mature and by means of mitosis give birth to spermatocytes I (2n), which will undergo meiosis.

7. What is the difference between spermatocyte I and spermatocyte II cells?

The spermatocyte I (2n) undergoes the first division of meiosis (meiosis I), producing two spermatocyte II (haploid, n) cells.

8. What is the difference between spermatocyte II and spermatid cells?

Spermatids (n) are the products of the second division of meiosis (meiosis II) during male gametogenesis. Each spermatocyte II produces two spermatids, totaling four spermatids for each spermatocyte I that undergoes meiosis.


9. What is the difference between spermatids and sperm cells? What is the name given to the transformation of spermatids into sperm cells?

Sperm cells (male gametes) are mature spermatids that have already undergone differentiation (the appearance of the flagellum, the reduction of the cytoplasm, the formation of the acrosome, the increase in the number of mitochondria). This differentiation process is called spermiogenesis.

10. What is the acrosome of the sperm cell? How is it formed?

The acrosome is a structure that contains a large number of digestive enzymes. It is located at the anterior end of the sperm cell and is formed through the union of Golgi apparatus vesicles. The function of the acrosome is to release its enzymes when the sperm cell meets the egg cell to break the external covering of the female gamete, thus making fertilization possible.

11. What is the function of the flagellum of the sperm cell? How is it formed?

The flagellum of the sperm cell is formed of the centrioles that migrate to the region posterior to the nucleus. Its function is to promote locomotion towards the egg cell.

12. Why is the cytoplasm of sperm cells very small? Why do the mitochondria of sperm cells concentrate at the base of the flagellum?

The reduced cytoplasm of sperm cells decreases the cell weight and provides a more hydrodynamic shape for its locomotion in fluids.

The high concentration of mitochondria at the base of the flagellum of the sperm cell is necessary for supplying energy to the flagellum (for it to vibrate and move the sperm cell).


13. Concerning events during the periods of life, how different is gametogenesis in women and in men?

The formation of spermatogonia in men takes place during the embryonic period. However, the formation of sperm cells is a continuous process that begins in puberty and goes on until old age, and sometimes during the whole life of the man.

In women, all oogonia are formed before birth. The oogonia turn into oocytes I, which enter the first division of meiosis (meiosis I). However, this division is interrupted at prophase and continues only in puberty. After the beginning of menses, an egg cell is released during each period and, if fertilized, it finishes its meiotic division. Oogenesis stops after menopause (cessation of menstrual activity) and the climacteric period of life begins.

14. Indicating the name and respective ploidy of each cell involved, how can the formation of egg cells from germ cells be described?

The formation of egg cells begins with a germ cell called an oogonium (2n), which undergoes mitosis and gives birth to the oocyte I (2n). The oocyte I undergoes meiosis I, but this is interrupted at prophase. After puberty, during each menstrual cycle, an oocyte I finishes meiosis I and generates one oocyte II (n) and the first polar body (n). With fertilization, the oocyte II then undergoes meiosis II and produces the mature egg cell (n) and the second polar body (n).

15. What is the first polar body? How different is it from an oocyte II?

In oogenesis, the oogonium differentiates into an oocyte I (2n) and this cell undergo meiosis. After finishing the first meiotic division (meiosis I), the oocyte I forms two cells: the oocyte II (n) and the first polar body. The oocyte II is bigger because it receives almost all the cytoplasm and the cytoplasmic structures of the oocyte I as a strategy for metabolite and nutrient storage. The oocyte II cell then undergoes the second meiotic division. The first polar body is very small and has almost no cytoplasm it either disintegrates or stays attached to the oocyte II.

16. What is the relationship between fertilization and the end of the meiotic process during oogenesis?

The oocyte II only completes the second meiotic division (interrupted at metaphase) if fertilization by a male gamete occurs. (Therefore, it can be said that the female gamete is the oocyte II).

17. What is the second polar body?

After the end of the second meiotic division of the oocyte II, two cells are generated: the egg cell and the second polar body. The second polar body is a very small cell that has almost no cytoplasm and which stays adnexal to the egg cell. The entire cytoplasmic content of the oocyte II passes on to the egg cell.


18. What is the relationship between the menstrual cycle and ovulation?

Ovulation is the releasing of the female gamete from the ovary. Ovulation is a periodical event that occurs during each menstrual cycle. Considering the day when menses begins the first day of the menstrual cycle ,  ovulation occurs around the 14th day, when the concentrations of the hormones LH and FSH reach high levels.


19. How does the male gamete penetrate the egg cell? How does the female gamete protect itself from the entrance of more gametes after the entrance of the first sperm cell?

The sperm cell that reaches the egg cell first triggers the acrosome reaction, a process in which hydrolytic enzymes of the acrosome are released on the external surface of the zona pellucida (the protective layer that surrounds the egg cell). A portion of this layer is digested by the acrosomal enzymes, allowing the sperm cell to reach the plasma membrane of the egg cell, thus fertilizing it.

At the moment that the sperm cell makes contact with the egg cell membrane, a chemical alteration of this membrane occurs. Enzymes secreted by exocytosis (a cortical reaction) make it impossible for the zona pellucida to bind to other sperm cells (zonal reaction) and, as a result, other male gametes cannot enter the egg cell.

20. What are the female pronucleus and the male pronucleus?

The female pronucleus is the haploid nucleus of the egg cell. the male pronucleus is the haploid nucleus of the sperm cell that has fertilized the egg cell. After fertilization, both pronuclei fuse, forming the nucleus of the diploid zygote.

21. Concerning their size and basic morphology, how and why are male and female gametes different from each other?

Female gametes are large cells full of vitellus (nutritional materials). Male gametes are small, mobile and agile flagellate cells.

These features are related to their respective biological functions. While female gametes have the basic functions of receiving the sperm cell nucleus and storing nutrients for the zygote, male gametes have the function of active movement towards the egg cell.

Now that you have finished studying Gametogenesis, these are your options:

What Happens Before Meiosis?

Before meiosis, the chromosomes in the nucleus of the cell replicate to produce double the amount of chromosomal material. After chromosomal replication, chromosomes separate into sister chromatids. This is known as interphase, and can be further broken down into two phases in the meiotic cycle: Growth (G), and Synthesis (S). During the G phase proteins and enzymes necessary for growth are synthesized, while during the S phase chromosomal material is doubled.

Meiosis is then split into two phases: meiosis I and meiosis II. In each of these phases, there is a prophase, a metaphase, and anaphase and a telophase. In meiosis I these are known as prophase I, metaphase I, anaphase I and telophase I, while in meiosis II they are known as prophase II, metaphase II, anaphase II and telophase II. Different products are formed by these phases, although the basic principles of each are the same. Also, meiosis I is preceded in interphase by both G phase and S phase, while meiosis II is only preceded by S phase: chromosomal replication is not necessary again.

How are germ cells not reduced in number? - Biology

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Reduction of germ cells yields more zebrafish males

Temasek Life Sciences Laboratory, Hokkaido University and Ehime University are pleased to announce that their researchers have discovered that the reduction of gonadal stem cells will yield more male zebrafish. The article reporting this finding has been published online in Stem Cell Reports today.

These results indicate that a certain number of these specialized gonadal stem cells (primordial germ cells or PGCs) is required for ovary formation. Reduced PGC numbers result in more males, as some of the females are forced to change their sex permanently without affecting their fertility, indicating that PGC count plays a regulatory role during sexual differentiation in zebrafish. The findings suggest that a stem cell counting mechanism in the zebrafish gonad is important for determining sexual development, which provides new insight in vertebrate germline biology.

The sex ratio of cultured stocks is an important aspect of aquaculture, as there are distinct differences (e.g. size, colour, maturation, etc.) between the two sexes in several fish species. This discovery may provide potential tools for improved sex control of fishes in farms in the future.

Brief Summary of Research

There are more fish species on Earth than all other vertebrates combined. Fishes are very diverse not only in their external appearance, but also in the way their sexual development is controlled. Zebrafish are small-bodied ornamental fish that have become an important model for vertebrate biology over the past four decades. Every zebrafish individual starts to develop as an immature female, and future males must undergo a 'gonadal transformation' to produce functional testes. The molecular regulation of this process appears to be complex and poorly understood.

In an article that appears online in Stem Cell Reports (Cell Press), researchers from Temasek Life Sciences Laboratory (Singapore) – in collaboration with Japanese scientists from Hokkaido University and Ehime University – reveal that the number of PGCs plays a regulatory role during sexual differentiation in zebrafish. Using different methods and zebrafish lines, they demonstrate that a reduction in the number of PGCs results in more males presumably by forcing some of the females to change their sex permanently without affecting their fertility.

"These data show that a PGC counting mechanism in the gonad determines sexual development, giving rise to the hypothesis of PGC dosage-dependent sex differentiation. This provides a novel perspective to research on sexual development of fishes and a new insight in vertebrate germline biology" – said Associate Professor Rie Goto at Ehime University.

"Better understanding of this 'gonadal switch' in zebrafish might eventually lead to improved tools for sex control in cultured fish species, especially in 'sex changing' food fishes, such as the groupers or Asian seabass, and improvements in their farm-based culture" – commented Professor László Orbán, Senior Principal Investigator at Temasek Life Sciences Laboratory.


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