Intragenomic conflict refers to the phenomenon where have phenotypic effects that promote their own transmission in detriment of the transmission of other genes that reside in the same genome.
Nuclear genes
Autosome genes usually have the same mode of transmission in sexually reproducing species due to the fairness of Mendelian segregation, but conflicts among
of autosomic genes may arise when an allele cheats during
gametogenesis (segregation distortion) or eliminates
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
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, 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 (
Drosophilidae),
haplotype in
Mus musculus (
mouse) and
sk in
Neurospora spp. (
fungus). Possible examples have also been reported in humans.
Segregation distorters that are present in sexual 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.
Killer and target
The simplest model of
meiotic drive involves two tightly linked loci: a
Killer locus and a
Target locus. The segregation distorter set is composed by the allele
Killer (in the
Killer locus) and the allele
Resistant (in the
Target locus), while its rival set is composed by the alleles
Non-killer and
Non-resistant. So, the segregation distorter set produces a toxin to which it is itself resistant, while its rival is not. Thus, it kills those gametes containing the rival set and increases in frequency. The tight linkage between these loci is crucial, so these genes usually lie on low-recombination regions of the genome.
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
(knobs) of maize, as well as several chromosomal rearrangements in mammals. The general molecular evolution of
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 (group I & II) and . 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
are nonessential
; 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
and
.
Cytoplasmic genes
Since nuclear and cytoplasmic genes usually have different modes of transmission, intragenomic conflicts between them may arise.
Mitochondria and chloroplasts are two examples of sets of cytoplasmic genes that commonly have exclusive maternal inheritance, similar to endosymbiont parasites in arthropods, like
Wolbachia.
Males as dead-ends to cytoplasmic genes
Anisogamy generally produces
zygotes that inherit cytoplasmic elements exclusively from the female gamete. Thus, males represent dead-ends to these genes. Because of this fact, cytoplasmic genes have evolved a number of mechanisms to increase the production of female descendants and eliminate offspring not containing them.
Feminization
Male organisms are converted into females by cytoplasmic inherited protists (
Microsporidia) or bacteria (
Wolbachia), regardless of nuclear sex-determining factors. This occurs in
Amphipoda and
Isopoda crustacean and
Lepidoptera.
Male-killing
Male
embryos (in the case of cytoplasmic inherited bacteria) or male
(in the case of Microsporidia) are killed. In the case of embryo death, this diverts investment from males to females who can transmit these cytoplasmic elements (for instance, in ladybird beetles, infected female hosts eat their dead male brothers, which is positive from the viewpoint of the bacterium). In the case of microsporidia-induced larval death, the agent is transmitted out of the male lineage (through which it cannot be transmitted) into the environment, where it may be taken up again infectiously by other individuals. Male-killing occurs in many
insects. In the case of male embryo death, a variety of bacteria have been implicated, including
Wolbachia.
Male-sterility
In some cases
anther tissue (male
gametophyte) is killed by
mitochondria in
monoecious angiosperms, increasing energy and material spent in developing female gametophytes. This leads to a shift from monoecy to
gynodioecy, where part of the plants in the population are male-sterile.
Parthenogenesis induction
In certain
haplodiploid Hymenoptera and
mites, in which males are produced asexually,
Wolbachia and
Cardinium can induce duplication of the
and thus convert the organisms into females. The cytoplasmic bacterium forces
haploid cells to go through incomplete mitosis to produce
diploid cells which therefore will be female. This produces an entirely female population. If antibiotics are administered to populations which have become asexual in this way, they revert to sexuality instantly, as the cytoplasmic bacteria forcing this behaviour upon them are removed.
Cytoplasmic incompatibility
In many
arthropods, zygotes produced by sperm of infected males and ova of non-infected females can be killed by
Wolbachia or
Cardinium.
Evolution of sex
Conflict between chromosomes has been proposed as an element in the evolution of sex.
[ See also [1].]
See also
Further reading
