Germ cell

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For the colloquial term for a disease causing agent, or other various meanings, see Germ (disambiguation).
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A germ cell is any cell that gives rise to the

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]

Introduction

Multicellular eukaryotes are made of two fundamental cell types: germ and somatic. Germ cells produce gametes and are the only cells that can undergo meiosis as well as mitosis. Somatic cells are all the other cells that form the building blocks of the body and they only divide by mitosis. The lineage of germ cells is called the germline. Germ cell specification begins during cleavage in many animals or in the epiblast during gastrulation in birds and mammals. After transport, involving passive movements and active migration, germ cells arrive at the developing gonads. In humans, sexual differentiation starts approximately 6 weeks after conception. The end-products of the germ cell cycle are the egg or sperm.[4]

Under special conditions

pluripotent in vitro, but only ESCs have proven pluripotency in vivo. Recent studies have demonstrated that it is possible to give rise to primordial germ cells from ESCs.[5]

Specification

There are two mechanisms to establish the germ cell lineage in the embryo. The first way is called preformistic and involves that the cells destined to become germ cells inherit the specific germ cell determinants present in the germ plasm (specific area of the cytoplasm) of the egg (ovum). The unfertilized egg of most animals is asymmetrical: different regions of the cytoplasm contain different amounts of mRNA and proteins.

The second way is found in mammals, where germ cells are not specified by such determinants but by signals controlled by zygotic genes. In mammals, a few cells of the early embryo are induced by signals of neighboring cells to become

totipotent. This means that they can differentiate in any cell type in the body and thus germ cells. Specification of primordial germ cells in the laboratory mouse is initiated by high levels of bone morphogenetic protein (BMP) signaling, which activates expression of the transcription factors Blimp-1/Prdm1 and Prdm14.[6]

It is speculated that induction was the ancestral mechanism, and that the preformistic, or inheritance, mechanism of germ cell establishment arose from convergent evolution.[7] There are several key differences between these two mechanisms that may provide reasoning for the evolution of germ plasm inheritance. One difference is that typically inheritance occurs almost immediately during development (around the blastoderm stage) while induction typically does not occur until gastrulation. As germ cells are quiescent and therefore not dividing, they are not susceptible to mutation.

Since the germ cell lineage is not established right away by induction, there is a higher chance for mutation to occur before the cells are specified. Mutation rate data is available that indicates a higher rate of germ line mutations in mice and humans, species which undergo induction, than in C. elegans and Drosophila melanogaster, species which undergo inheritance.[8] A lower mutation rate would be selected for, which is one possible reason for the convergent evolution of the germ plasm. However, more mutation rate data will need to be collected across several taxa, particularly data collected both before and after the specification of primordial germ cells before this hypothesis on the evolution of germ plasm can be backed by strong evidence.

Migration

Main article: Primordial germ cell migration

Primordial germ cells, germ cells that still have to reach the gonads (also known as PGCs, precursor germ cells or gonocytes) divide repeatedly on their migratory route through the gut and into the developing gonads.[9]

Invertebrates

In the

chemoattractants, stimulate the migration in the gonadal mesoderm.[citation needed
]

Vertebrates

In the acquatic frog

vegetal blastomeres. These presumptive PGCs are brought to the endoderm of the blastocoel by gastrulation. They are determined as germ cells when gastrulation is completed. Migration from the hindgut along the gut and across the dorsal mesentery then takes place. The germ cells split into two populations and move to the paired gonadal ridges. Migration starts with 3-4 cells that undergo three rounds of cell division so that about 30 PGCs arrive at the gonads. On the migratory path of the PGCs, the orientation of underlying cells and their secreted molecules such as fibronectin play an important role.[citation needed
]

Mammals have a migratory path comparable to that in Xenopus. Migration begins with 50 gonocytes and about 5,000 PGCs arrive at the gonads. Proliferation occurs also during migration and lasts for 3–4 weeks in humans.[citation needed]

PGCs come from the epiblast and migrate subsequently into the mesoderm, the endoderm and the posterior of the yolk sac. Migration then takes place from the hindgut along the gut and across the dorsal mesentery to reach the gonads (4.5 weeks in human beings). Fibronectin maps here also a polarized network together with other molecules. The somatic cells on the path of germ cells provide them attractive, repulsive, and survival signals. But germ cells also send signals to each other.[citation needed]

In

chemoattractants are probably involved in helping PGCs migrate.[citation needed
]

The Sry gene of the Y chromosome

The

testes or ovaries results in the development of a female, independent of the carried sex chromosome.[10]

Retinoic Acid and Germ cell differentiation

Retinoic acid (RA) is an important factor that causes differentiation of primordial germ cells. In males, the mesonephros releases retinoic acid. RA then goes to the gonad causing an enzyme called CYP26B1 to be released by sertoli cells. CYP26B1 metabolizes RA, and because sertoli cells surround primordial germ cells (PGCs), PGCs never come into contact with RA, which results in a lack of proliferation of PGCs and no meiotic entry. This keeps spermatogenesis from starting too soon. In females, the mesonephros releases RA, which enters the gonad. RA stimulates Stra8, a critical gatekeeper of meiosis (1), and Rec8, causing primordial germ cells to enter meiosis. This causes the development of oocytes that arrest in meiosis I.[11]

Gametogenesis

haploid eggs or sperm (respectively oogenesis and spermatogenesis) is different for each species but the general stages are similar. Oogenesis and spermatogenesis
have many features in common, they both involve:

  • Meiosis
  • Extensive morphological differentiation
  • Incapacity of surviving for very long if fertilization does not occur

Despite their homologies they also have major differences:[citation needed]

  • Spermatogenesis has equivalent meiotic divisions resulting in four equivalent
    polar bodies
    .
  • Different timing of maturation: oogenic meiosis is interrupted at one or more stages (for a long time) while spermatogenic meiosis is rapid and uninterrupted.

Oogenesis

After migration primordial germ cells will become oogonia in the forming gonad (ovary). The oogonia proliferate extensively by mitotic divisions, up to 5-7 million cells in humans. But then many of these oogonia die and about 50,000 remain. These cells differentiate into primary oocytes. In week 11-12 post coitus the first meiotic division begins (before birth for most mammals) and remains arrested in prophase I from a few days to many years depending on the species. It is in this period or in some cases at the beginning of sexual maturity that the primary oocytes secrete proteins to form a coat called

haploid cells. The polar bodies degenerate.[12] Oocyte maturation stands by at metaphase II in most vertebrates. During ovulation, the arrested secondary oocyte leaves the ovary and matures rapidly into an egg ready for fertilization. Fertilization will cause the egg to complete meiosis II. In human females there is proliferation of the oogonia in the fetus, meiosis starts then before birth and stands by at meiotic division I up to 50 years, ovulation begins at puberty.[citation needed
]

Egg growth

A 10 - 20 μm large somatic cell generally needs 24 hours to double its

accessory cells in the ovary can also provide nutritive help of two types. In some invertebrates some oogonia become nurse cells. These cells are connected by cytoplasmic bridges with oocytes. The nurse cells of insects provide oocytes macromolecules such as proteins and mRNA. Follicular granulosa cells are the second type of accessory cells in the ovary in both invertebrates and vertebrates. They form a layer around the oocyte and nourish them with small molecules, no macromolecules, but eventually their smaller precursor molecules, by gap junctions.[citation needed
]

Mutation and DNA repair

The mutation frequency of female germline cells in mice is about 5-fold lower than that of somatic cells, according to one study.[13]

The mouse

leptotene, zygotene and pachytene) stages of meiosis.[14] The long period of meiotic arrest at the four chromatid dictyate stage of meiosis may facilitate recombinational repair of DNA damages.[15]

Spermatogenesis

seminiferous tubules in the testicles and go on continuously. Spermatogonia are immature germ cells. They proliferate continuously by mitotic divisions around the outer edge of the seminiferous tubules, next to the basal lamina. Some of these cells stop proliferation and differentiate into primary spermatocytes. After they proceed through the first meiotic division, two secondary spermatocytes are produced. The two secondary spermatocytes undergo the second meiotic division to form four haploid spermatids. These spermatids differentiate morphologically into sperm by nuclear condensation, ejection of the cytoplasm and formation of the acrosome and flagellum.[citation needed
]

The developing male germ cells do not complete cytokinesis during spermatogenesis. Consequently, cytoplasmic bridges exist during interphase to ensure connection between the clones of differentiating daughter cells. These bridges are called a syncytium, and feature a TEX14 and KIF23 ring in their centre.[16][17] In this way the haploid cells are supplied with all the products of a complete diploid genome. Sperm that carry a Y chromosome, for example, are supplied with essential molecules that are encoded by genes on the X chromosome.[citation needed]

Success of germ cell proliferation and differentiation is also ensured by a balance between germ cell development and programmed cell death. Identification of «death triggering signals» and corresponding receptor proteins is important for the fertilization potential of males. Apoptosis in germ cells can be induced by variety of naturally occurring toxicant. Receptors belonging to the taste 2 family are specialized to detect bitter compounds including extremely toxic alkaloids. So taste receptors play a functional role for controlling apoptosis in male reproductive tissue.[18]

Mutation and DNA repair

The mutation frequencies for cells throughout the different stages of spermatogenesis in mice is similar to that in female germline cells, that is 5 to 10-fold lower than the mutation frequency in somatic cells[19][13] Thus low mutation frequency is a feature of germline cells in both sexes. Homologous recombinational repair of double-strand breaks occurs in mouse during sequential stages of spermatogenesis, but is most prominent in spermatocytes.[15] The lower frequencies of mutation in germ cells compared to somatic cells appears to be due to more efficient removal of DNA damages by repair processes including homologous recombination repair during meiosis.[20] Mutation frequency during spermatogenesis increases with age.[19] The mutations in spermatogenic cells of old mice include an increased prevalence of transversion mutations compared to young and middle-aged mice.[21]

Diseases

Germ cell tumor is a rare cancer that can affect people at all ages. As of 2018, germ cell tumors account for 3% of all cancers in children and adolescents 0–19 years old.[22]

Germ cell tumors are generally located in the

malignant.[23]

On arrival at the gonad, primordial germ cells that do not properly differentiate may produce

mouse model.[24]

Induced differentiation

Inducing differentiation of certain cells to germ cells has many applications. One implication of induced differentiation is that it may allow for the eradication of male and female factor infertility. Furthermore, it would allow same-sex couples to have biological children if sperm could be produced from female cells or if eggs could be produced from male cells. Efforts to create sperm and eggs from skin and embryonic stem cells were pioneered by Hayashi and Saitou's research group at Kyoto University.[25] These researchers produced primordial germ cell-like cells (PGLCs) from embryonic stem cells (ESCs) and skin cells in vitro.

Hayashi and Saitou's group was able to promote the differentiation of embryonic stem cells into PGCs with the use of precise timing and bone morphogenetic protein 4 (Bmp4). Upon succeeding with embryonic stem cells, the group was able to successfully promote the differentiation of induced pluripotent stem cells (iPSCs) into PGLCs. These primordial germ cell-like cells were then used to create spermatozoa and oocytes.[26]

Efforts for human cells are less advanced due to the fact that the PGCs formed by these experiments are not always viable. In fact Hayashi and Saitou's method is only one third as effective as current in vitro fertilization methods, and the produced PGCs are not always functional. Furthermore, not only are the induced PGCs not as effective as naturally occurring PGCs, but they are also less effective at erasing their epigenetic markers when they differentiate from iPSCs or ESCs to PGCs.

There are also other applications of induced differentiation of germ cells. Another study showed that culture of

human embryonic stem cells in mitotically inactivated porcine ovarian fibroblasts (POF) causes differentiation into germ cells, as evidenced by gene expression analysis.[27]

See also

References

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External links

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