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Germline

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In biology and genetics, the germline is the population of a multicellular organism's cells that develop into germ cells. In other words, they are the cells that form gametes (eggs and sperm), which can come together to form a zygote. They differentiate in the gonads from primordial germ cells into gametogonia, which develop into gametocytes, which develop into the final gametes.[1] This process is known as gametogenesis.

Cormlets of Watsonia meriana, an example of apomixis
Clathria tuberosa, an example of a sponge that can grow indefinitely from somatic tissue and reconstitute itself from totipotent separated somatic cells

Germ cells pass on genetic material through the process of sexual reproduction. This includes fertilization, recombination and meiosis. These processes help to increase genetic diversity in offspring.[2]

Certain organisms reproduce asexually via processes such as apomixis, parthenogenesis, autogamy, and cloning.[3][4] Apomixis and Parthenogenesis both refer to the development of an embryo without fertilization. The former typically occurs in plants seeds, while the latter tends to be seen in nematodes, as well as certain species of reptiles, birds, and fish.[5][6] Autogamy is a term used to describe self pollination in plants.[7] Cloning is a technique used to creation of genetically identical cells or organisms.[8]

In sexually reproducing organisms, cells that are not in the germline are called somatic cells. According to this definition, mutations, recombinations and other genetic changes in the germline may be passed to offspring, but changes in a somatic cell will not be.[9] This need not apply to somatically reproducing organisms, such as some Porifera[10] and many plants. For example, many varieties of citrus,[11] plants in the Rosaceae and some in the Asteraceae, such as Taraxacum, produce seeds apomictically when somatic diploid cells displace the ovule or early embryo.[12]

In an earlier stage of genetic thinking, there was a clear distinction between germline and somatic cells. For example, August Weismann proposed and pointed out, a germline cell is immortal in the sense that it is part of a lineage that has reproduced indefinitely since the beginning of life and, barring accident, could continue doing so indefinitely.[13] However, it is now known in some detail that this distinction between somatic and germ cells is partly artificial and depends on particular circumstances and internal cellular mechanisms such as telomeres and controls such as the selective application of telomerase in germ cells, stem cells and the like.[14]

Not all multicellular organisms differentiate into somatic and germ lines,[15] but in the absence of specialised technical human intervention practically all but the simplest multicellular structures do so. In such organisms somatic cells tend to be practically totipotent, and for over a century sponge cells have been known to reassemble into new sponges after having been separated by forcing them through a sieve.[10]

Germline can refer to a lineage of cells spanning many generations of individuals—for example, the germline that links any living individual to the hypothetical last universal common ancestor, from which all plants and animals descend.

Evolution

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Plants and basal metazoans such as sponges (Porifera) and corals (Anthozoa) do not sequester a distinct germline, generating gametes from multipotent stem cell lineages that also give rise to ordinary somatic tissues. It is therefore likely that germline sequestration first evolved in complex animals with sophisticated body plans, i.e. bilaterians. There are several theories on the origin of the strict germline-soma distinction. Setting aside an isolated germ cell population early in embryogenesis might promote cooperation between the somatic cells of a complex multicellular organism.[16] Another recent theory suggests that early germline sequestration evolved to limit the accumulation of deleterious mutations in mitochondrial genes in complex organisms with high energy requirements and fast mitochondrial mutation rates.[15]

DNA damage, mutation and repair

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Reactive oxygen species (ROS) are produced as byproducts of metabolism. In germline cells, ROS are likely a significant cause of DNA damages that, upon DNA replication, lead to mutations. 8-Oxoguanine, an oxidized derivative of guanine, is produced by spontaneous oxidation in the germline cells of mice, and during the cell's DNA replication cause GC to TA transversion mutations.[17] Such mutations occur throughout the mouse chromosomes as well as during different stages of gametogenesis.

The mutation frequencies for cells in different stages of gametogenesis are about 5 to 10-fold lower than in somatic cells both for spermatogenesis[18] and oogenesis.[19] The lower frequencies of mutation in germline cells compared to somatic cells appears to be due to more efficient DNA repair of DNA damages, particularly homologous recombinational repair, during germline meiosis.[20] Among humans, about five percent of live-born offspring have a genetic disorder, and of these, about 20% are due to newly arisen germline mutations.[18]

Epigenetic alterations

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5 methylcytosine methyl highlight. The image shows a cytosine single ring base and a methyl group added on to the 5 carbon. In mammals, DNA methylation occurs almost exclusively at a cytosine that is followed by a guanine.

Epigenetic alterations of DNA include modifications that affect gene expression, but are not caused by changes in the sequence of bases in DNA. A well-studied example of such an alteration is the methylation of DNA cytosine to form 5-methylcytosine. This usually occurs in the DNA sequence CpG, changing the DNA at the CpG site from CpG to 5-mCpG. Methylation of cytosines in CpG sites in promoter regions of genes can reduce or silence gene expression.[21] About 28 million CpG dinucleotides occur in the human genome,[22] and about 24 million CpG sites in the mouse genome (which is 86% as large as the human genome[23]). In most tissues of mammals, on average, 70% to 80% of CpG cytosines are methylated (forming 5-mCpG).[24]

In the mouse, by days 6.25 to 7.25 after fertilization of an egg by a sperm, cells in the embryo are set aside as primordial germ cells (PGCs). These PGCs will later give rise to germline sperm cells or egg cells. At this point the PGCs have high typical levels of methylation. Then primordial germ cells of the mouse undergo genome-wide DNA demethylation, followed by subsequent new methylation to reset the epigenome in order to form an egg or sperm.[25]

In the mouse, PGCs undergo DNA demethylation in two phases. The first phase, starting at about embryonic day 8.5, occurs during PGC proliferation and migration, and it results in genome-wide loss of methylation, involving almost all genomic sequences. This loss of methylation occurs through passive demethylation due to repression of the major components of the methylation machinery.[25] The second phase occurs during embryonic days 9.5 to 13.5 and causes demethylation of most remaining specific loci, including germline-specific and meiosis-specific genes. This second phase of demethylation is mediated by the TET enzymes TET1 and TET2, which carry out the first step in demethylation by converting 5-mC to 5-hydroxymethylcytosine (5-hmC) during embryonic days 9.5 to 10.5. This is likely followed by replication-dependent dilution during embryonic days 11.5 to 13.5.[26] At embryonic day 13.5, PGC genomes display the lowest level of global DNA methylation of all cells in the life cycle.[25]

In the mouse, the great majority of differentially expressed genes in PGCs from embryonic day 9.5 to 13.5, when most genes are demethylated, are upregulated in both male and female PGCs.[26]

Following erasure of DNA methylation marks in mouse PGCs, male and female germ cells undergo new methylation at different time points during gametogenesis. While undergoing mitotic expansion in the developing gonad, the male germline starts the re-methylation process by embryonic day 14.5. The sperm-specific methylation pattern is maintained during mitotic expansion. DNA methylation levels in primary oocytes before birth remain low, and re-methylation occurs after birth in the oocyte growth phase.[25]

See also

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References

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  1. ^ Yao, Chunmeng; Yao, Ruqiang; Luo, Haining; Shuai, Ling (2022). "Germline specification from pluripotent stem cells". Stem Cell Research & Therapy. 13 (1): 74. doi:10.1186/s13287-022-02750-1. PMC 8862564. PMID 35189957.
  2. ^ Zickler, Denise; Kleckner, Nancy (2015). "Recombination, Pairing, and Synapsis of Homologs during Meiosis". Cold Spring Harbor Perspectives in Biology. 7 (6): a016626. doi:10.1101/cshperspect.a016626. PMC 4448610. PMID 25986558.
  3. ^ Tarín, Juan J.; Cano, Antonio, eds. (2000). Fertilization in protozoa and metazoan animals: cellular and molecular aspects. Berlin Heidelberg: Springer. ISBN 978-3-540-67093-3.
  4. ^ Lowe, Andrew; Harris, Stephen; Ashton, Paul (1 April 2000). Ecological Genetics: Design, Analysis, and Application. John Wiley & Sons. ISBN 978-1-444-31121-1.
  5. ^ Niccolò, Terzaroli; Anderson, Aaron W.; Emidio, Albertini (2023). "Apomixis: oh, what a tangled web we have!". Planta. 257 (5): 92. Bibcode:2023Plant.257...92N. doi:10.1007/s00425-023-04124-0. PMC 10066125. PMID 37000270.
  6. ^ Dudgeon, Christine L.; Coulton, Laura; Bone, Ren; Ovenden, Jennifer R.; Thomas, Severine (2017). "Switch from sexual to parthenogenetic reproduction in a zebra shark". Scientific Reports. 7 (1): 40537. Bibcode:2017NatSR...740537D. doi:10.1038/srep40537. PMC 5238396. PMID 28091617.
  7. ^ Eckert, Christopher G. (February 2000). "Contributions of Autogamy and Geitonogamy to Self-Fertilization in a Mass-Flowering, Clonal Plant". Ecology. 81 (2). Ecological Society of America: 532–542. doi:10.1890/0012-9658(2000)081[0532:COAAGT]2.0.CO;2. ISSN 0012-9658 – via John Wiley and Sons.
  8. ^ Bonetti, G.; Donato, K.; Medori, M. C.; Dhuli, K.; Henehan, G.; Brown, R.; Sieving, P.; Sykora, P.; Marks, R.; Falsini, B.; Capodicasa, N.; Miertus, S.; Lorusso, L.; Dondossola, D.; Tartaglia, G. M. (2023). "Human Cloning: Biology, Ethics, and Social Implications". La Clinica Terapeutica (in Italian). 174 (6). doi:10.7417/ct.2023.2492.
  9. ^ C.Michael Hogan. 2010. Mutation. ed. E.Monosson and C.J.Cleveland. Encyclopedia of Earth. National Council for Science and the Environment. Washington DC Archived April 30, 2011, at the Wayback Machine
  10. ^ a b Brusca, Richard C.; Brusca, Gary J. (1990). Invertebrates. Sunderland: Sinauer Associates. ISBN 978-0878930982.
  11. ^ Akira Wakana and Shunpei Uemoto. Adventive Embryogenesis in Citrus (Rutaceae). II. Postfertilization Development. American Journal of Botany Vol. 75, No. 7 (Jul., 1988), pp. 1033-1047 Published by: Botanical Society of America Article Stable URL: https://www.jstor.org/stable/2443771
  12. ^ K V Ed Peter (5 February 2009). Basics Of Horticulture. New India Publishing. pp. 9–. ISBN 978-81-89422-55-4.
  13. ^ August Weismann (1892). Essays upon heredity and kindred biological problems. Clarendon press.
  14. ^ Watt, F. M. and B. L. M. Hogan. 2000 Out of Eden: Stem Cells and Their Niches Science 287:1427-1430.
  15. ^ a b Radzvilavicius, Arunas L.; Hadjivasiliou, Zena; Pomiankowski, Andrew; Lane, Nick (2016-12-20). "Selection for Mitochondrial Quality Drives Evolution of the Germline". PLOS Biology. 14 (12): e2000410. doi:10.1371/journal.pbio.2000410. ISSN 1545-7885. PMC 5172535. PMID 27997535.
  16. ^ Buss, L W (1983-03-01). "Evolution, development, and the units of selection". Proceedings of the National Academy of Sciences of the United States of America. 80 (5): 1387–1391. Bibcode:1983PNAS...80.1387B. doi:10.1073/pnas.80.5.1387. ISSN 0027-8424. PMC 393602. PMID 6572396.
  17. ^ Ohno M, Sakumi K, Fukumura R, Furuichi M, Iwasaki Y, Hokama M, Ikemura T, Tsuzuki T, Gondo Y, Nakabeppu Y (2014). "8-oxoguanine causes spontaneous de novo germline mutations in mice". Sci Rep. 4: 4689. Bibcode:2014NatSR...4E4689O. doi:10.1038/srep04689. PMC 3986730. PMID 24732879.
  18. ^ a b Walter CA, Intano GW, McCarrey JR, McMahan CA, Walter RB (1998). "Mutation frequency declines during spermatogenesis in young mice but increases in old mice". Proc. Natl. Acad. Sci. U.S.A. 95 (17): 10015–9. Bibcode:1998PNAS...9510015W. doi:10.1073/pnas.95.17.10015. PMC 21453. PMID 9707592.
  19. ^ Murphey P, McLean DJ, McMahan CA, Walter CA, McCarrey JR (2013). "Enhanced genetic integrity in mouse germ cells". Biol. Reprod. 88 (1): 6. doi:10.1095/biolreprod.112.103481. PMC 4434944. PMID 23153565.
  20. ^ Bernstein H, Byerly HC, Hopf FA, Michod RE. Genetic damage, mutation, and the evolution of sex. Science. 1985 Sep 20;229(4719):1277-81. doi: 10.1126/science.3898363. PMID 3898363
  21. ^ Bird A (January 2002). "DNA methylation patterns and epigenetic memory". Genes Dev. 16 (1): 6–21. doi:10.1101/gad.947102. PMID 11782440.
  22. ^ Lövkvist C, Dodd IB, Sneppen K, Haerter JO (June 2016). "DNA methylation in human epigenomes depends on local topology of CpG sites". Nucleic Acids Res. 44 (11): 5123–32. doi:10.1093/nar/gkw124. PMC 4914085. PMID 26932361.
  23. ^ Guénet JL (December 2005). "The mouse genome". Genome Res. 15 (12): 1729–40. doi:10.1101/gr.3728305. PMID 16339371.
  24. ^ Jabbari K, Bernardi G (May 2004). "Cytosine methylation and CpG, TpG (CpA) and TpA frequencies". Gene. 333: 143–9. doi:10.1016/j.gene.2004.02.043. PMID 15177689.
  25. ^ a b c d Zeng Y, Chen T (March 2019). "DNA Methylation Reprogramming during Mammalian Development". Genes (Basel). 10 (4): 257. doi:10.3390/genes10040257. PMC 6523607. PMID 30934924.
  26. ^ a b Yamaguchi S, Hong K, Liu R, Inoue A, Shen L, Zhang K, Zhang Y (March 2013). "Dynamics of 5-methylcytosine and 5-hydroxymethylcytosine during germ cell reprogramming". Cell Res. 23 (3): 329–39. doi:10.1038/cr.2013.22. PMC 3587712. PMID 23399596.
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