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Inbiology andgenetics, thegermline is the population of amulticellular organism's cells that develop intogerm cells. In other words, they are the cells that formgametes (eggs andsperm), which can come together to form azygote. They differentiate in thegonads fromprimordial germ cells intogametogonia, which develop intogametocytes, which develop into the final gametes.[1] This process is known asgametogenesis.
Germ cells pass on genetic material through the process of sexual reproduction. This includesfertilization,recombination andmeiosis. These processes help to increase genetic diversity in offspring.[2]
Certain organisms reproduce asexually via processes such asapomixis,parthenogenesis,autogamy, andcloning.[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 calledsomatic 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 somePorifera[10] and many plants. For example, many varieties ofcitrus,[11] plants in theRosaceae and some in theAsteraceae, such asTaraxacum, produce seeds apomictically when somaticdiploid 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 astelomeres and controls such as the selective application oftelomerase in germ cells,stem cells and the like.[14]
Not all multicellular organismsdifferentiate 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 practicallytotipotent, 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 hypotheticallast universal common ancestor, from which all plants and animalsdescend.
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]
Reactive oxygen species (ROS) are produced as byproducts of metabolism. In germline cells, ROS are likely a significant cause ofDNA damages that, uponDNA replication, lead tomutations.8-Oxoguanine, an oxidized derivative ofguanine, is produced by spontaneous oxidation in the germline cells of mice, and during the cell's DNA replication cause GC to TAtransversion mutations.[17] Such mutations occur throughout the mousechromosomes as well as during different stages ofgametogenesis.
The mutation frequencies for cells in different stages of gametogenesis are about 5 to 10-fold lower than insomatic cells both forspermatogenesis[18] andoogenesis.[19] The lower frequencies of mutation in germline cells compared to somatic cells appears to be due to more efficientDNA repair of DNA damages, particularlyhomologous recombinational repair, during germlinemeiosis.[20] Among humans, about five percent of live-born offspring have a genetic disorder, and of these, about 20% are due to newly arisengermline mutations.[18]
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 themethylation of DNA cytosine to form5-methylcytosine. This usually occurs in the DNA sequenceCpG, changing the DNA at theCpG site from CpG to 5-mCpG. Methylation of cytosines in CpG sites inpromoter 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 DNAdemethylation, followed by subsequent new methylation to reset theepigenome 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, involvingalmost 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 theTET enzymes TET1 and TET2, which carry out the first step in demethylation by converting 5-mC to5-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]
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