Intragenomic conflict

Nuclear genes

Autosomic genes usually have the same mode of transmission in sexually reproducing species due to the fairness of Mendelian segregation, but conflicts among alleles of autosomic genes may arise when an allele cheats during gametogenesis (segregation distortion) or eliminates embryos that do not contain it (lethal maternal effects). An allele may also directly convert its rival allele into a copy of itself (homing endonucleases). Finally, mobile genetic elements completely bypass Mendelian segregation, being able to insert new copies of themselves into new positions in the genome (transposons).

Segregation distortion

In principle, the two parental alleles have equal probabilities of being present in the mature gamete. However, there are several mechanisms that lead to an unequal transmission of parental alleles from parents to offspring. One example is a gene drive complex, called a Segregation Distorter (SD), that "cheats" during meiosis or gametogenesis and thus is present in more than half of the functional gametes. The most studied examples are SD in Drosophila melanogaster (fruit fly), t haplotype in Mus musculus (mouse) and sk in Neurospora spp. (fungus). Possible examples have also been reported in humans. Segregation distorters that are present on sex chromosomes (as is the case with the X chromosome in several Drosophila species) are denominated sex-ratio distorters, as they induce a sex-ratio bias in the offspring of the carrier individual.

Gamete killing

Gamete killers, a type of meiotic driver, are the most commonly identified type of segregation distorter. Gamete killers are often referred to as sperm killers, pollen killers, or spore killers depending on the clade in which they are found. They are most commonly expressed in males though there is one system in mice that appears to act via egg sabotage during female gametogenesis. Most gamete killer systems can be grouped into two sub groups: Driver-Target systems and Toxin-Antidote systems. In Driver-Target systems, the driving chromosome (containing the main drive locus and insensitive target locus) targets wild type chromosomes that contain a sensitive target locus. Importantly in this kind of system, recombination between the driver and target is often suppressed to avoid the formation of a "suicide chromosome". An example of a Driver-Target system is the coadapted gene complex in Drosophila melanogaster called Segregation Distorter (SD). The main drive locus, a truncated tandem duplication of the gene RanGAP on chromosome 2L (Sd-RanGAP) targets a repetitive array of satellite DNA on chromosome 2R called Responder. The mechanism of SD is unknown, but through some interaction with Responder, Sd-RanGAP induces a chromatin condensation defect in wild type sperm that results in their elimination. Toxin-Antidote systems on the other hand consist of a drive locus that produces both a toxin and an antidote. The toxin is fatal to gametes that do not contain the antidote which results in the death of those gametes. Spore killers, like sk and wtf, are frequently Toxin-Antidote systems.

True meiotic drive

Other systems do not involve gamete destruction, but rather use the asymmetry of meiosis in females: the driving allele ends up in the oocyte instead of in the polar bodies with a probability greater than one half. This is termed true meiotic drive, as it does not rely on a post-meiotic mechanism. The best-studied examples include the neocentromeres (knobs) of maize, as well as several chromosomal rearrangements in mammals. The general molecular evolution of centromeres is likely to involve such mechanisms.

Lethal maternal effects

The Medea gene causes the death of progeny from a heterozygous mother that do not inherit it. It occurs in the flour beetle (Tribolium castaneum). Maternal-effect selfish genes have been successfully synthesized in the lab.

Transposons

Transposons are autonomous replicating genes that encode the ability to move to new positions in the genome and therefore accumulate in the genomes. They replicate themselves in spite of being detrimental to the rest of the genome. They are often called 'jumping genes' or parasitic DNA and were discovered by Barbara McClintock in 1944.

Homing endonuclease genes

Homing endonuclease genes (HEG) convert their rival allele into a copy of themselves, and are thus inherited by nearly all meiotic daughter cells of a heterozygote cell. They achieve this by encoding an endonuclease which breaks the rival allele. This break is repaired by using the sequence of the HEG as template.

HEGs encode sequence-specific endonucleases. The recognition sequence (RS) is 15–30 bp long and usually occurs once in the genome. HEGs are located in the middle of their own recognition sequences. Most HEGs are encoded by self-splicing introns (group I & II) and inteins. Inteins are internal protein fragments produced from protein splicing and usually contain endonuclease and splicing activities. The allele without the HEGs are cleaved by the homing endonuclease and the double-strand break are repaired by homologous recombination (gene conversion) using the allele containing HEGs as template. Both chromosomes will contain the HEGs after repair.

B-chromosome

B-chromosomes are nonessential chromosomes; not homologous with any member of the normal (A) chromosome set; morphologically and structurally different from the As; and they are transmitted at higher-than-expected frequencies, leading to their accumulation in progeny. In some cases, there is strong evidence to support the contention that they are simply selfish and that they exist as parasitic chromosomes. They are found in all major taxonomic groupings of both plants and animals.