In biology and genetics, the germline in a multicellular organism is the population of its bodily cells that are so differentiated or segregated that in the usual processes of reproduction they may pass on their genetic material to the progeny.[1]

As a rule this passing-on happens via a process of sexual reproduction; typically it is a process that includes systematic changes to the genetic material, changes that arise during recombination, meiosis and fertilization for example. However, there are many exceptions, including processes and concepts such as various forms of apomixis, autogamy, automixis, cloning, or parthenogenesis.[2][3] The cells of the germline commonly are called germ cells.[4]

For example, gametes such as the sperm or the egg are part of the germline. So are the cells that divide to produce the gametes, called gametocytes, the cells that produce those, called gametogonia, and all the way back to the zygote, the cell from which the individual developed.[4]

In sexually reproducing organisms, cells that are not in the germline are called somatic cells. According to this view mutations, recombinations and other genetic changes in the germline may be passed to offspring, but a change in a somatic cell will not be.[5] This need not apply to somatically reproducing organisms, such as some Porifera[6] and many plants. For example, many varieties of citrus,[7] 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.[8]

In an earlier stage of genetic thinking, the distinction between germline and somatic cell was clear cut. 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.[9] 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.[10]

Not all multicellular organisms differentiate into somatic and germ lines,[11] 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.[6]

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.


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.[12] 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.[11]

DNA damage, mutation and repair

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.[13] 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 [14] and oogenesis.[15] 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. 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.[14]

See also


  1. Pieter Dirk Nieuwkoop; Lien A. Sutasurya (1979). Primordial Germ Cells in the Chordates: Embryogenesis and Phylogenesis. CUP Archive. ISBN 978-0-521-22303-4.
  2. Juan J. Tarin; Antonio Cano (14 September 2000). Fertilization in Protozoa and Metazoan Animals: Cellular and Molecular Aspects. Springer. ISBN 978-3-540-67093-3.
  3. Andrew Lowe; Stephen Harris; Paul Ashton (1 April 2009). Ecological Genetics: Design, Analysis, and Application. John Wiley & Sons. pp. 108–. ISBN 978-1-4443-1121-1.
  4. Nikolas Zagris; Anne Marie Duprat; Antony Durston (30 November 1995). Organization of the Early Vertebrate Embryo. Springer. pp. 2–. ISBN 978-0-306-45132-4.
  5. 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
  6. Brusca, Richard C.; Brusca, Gary J. (1990). Invertebrates. Sunderland: Sinauer Associates. ISBN 978-0878930982.
  7. 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:
  8. K V Ed Peter (5 February 2009). Basics Of Horticulture. New India Publishing. pp. 9–. ISBN 978-81-89422-55-4.
  9. August Weismann (1892). Essays upon heredity and kindred biological problems. Clarendon press.
  10. Watt, F. M. and B. L. M. Hogan. 2000 Out of Eden: Stem Cells and Their Niches Science 287:1427-1430.
  11. 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.
  12. 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. doi:10.1073/pnas.80.5.1387. ISSN 0027-8424. PMC 393602. PMID 6572396.
  13. 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. doi:10.1038/srep04689. PMC 3986730. PMID 24732879.
  14. 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. doi:10.1073/pnas.95.17.10015. PMC 21453. PMID 9707592.
  15. 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.
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