[1] It can occur during meiosis or replication of DNA, as well as due to ionizing or UV radiation, transposons, mutagenic chemicals, viruses and a number of other factors.
[1][5] It is theorized that these mutations, along with genetic recombination, are the raw material upon which natural selection can act to form evolutionary processes.
In other cases, they can help us understand how important patterns of behaviour were able to arise – on the back of a simple gene mutation.
[10][11] Finally, they can help provide key insight on the nature of speciation events which can occur when a behaviour mutation changes the courtship methods and manner of mating in sexually reproducing species.
The pioneers of the field include Dutch biologist Nikolaas Tinbergen and Austrian biologists Karl von Frisch and Konrad Lorenz[13][14][15] (the three won the Nobel Prize in Physiology or Medicine in 1973 for their discoveries concerning organization and elicitation of individual and social behaviour patterns).
[16] However, the first published demonstration of how a mutation in a single gene could change an organism's behaviour was carried out by Margaret Bastock in 1956, while she was a Ph.D. student working under Tinbergen at Oxford University.
Even after significant generations of crossing, the flies homozygous for the "yellow" allele were less successful in mating with wild type females than their heterozygous brothers.
These results led Bastock to conclude that the origin of this deficient mating behaviour was the very same mutant gene that caused yellow discolouration.
[17] In order to understand how behaviour is controlled by the nervous system, it is key to identify the neuronal substrates important for the specific activity studied, as well as to explain how they are incorporated into a functional circuit.
When shi was tested to cholinergic neurons, the flies showed a quick response to the temperature and were paralyzed within two minutes at 30 degrees, which was reversible.
This research will further be helpful in studying the neuronal subsets in the behaviour of intact animals due to the reversible and controlled manner it is performed in.
In more recent studies the Zebrafish ennui mutation was identified from mutagenesis identification for defects in early behaviour.
The acetylcholine receptor was significantly reduced in the adult ennui in size as well as localization at the myotome segment borders of fast-twitch muscles.
Genetic mosaic analysis revealed that ennui is necessary cell autonomously in muscle fibers for normal synaptic localization of acetylcholine receptors.
Spontaneous mutations play a central role in the maintenance of genetic variation and persistence of natural population of many organisms.
Phenotypic assays significantly determine whether and how quickly population with accumulated deleterious mutational loads can result in degradation of behavioural responses over time.
[1] Based on laboratory experimental evolution with long-term mutation accumulation (MA) lines of the nematode Caenorhabditis elegans, a team of researchers at the University of Oregon investigated that mutation accumulation of behaviour is capable of generating significant levels of individual variation in ecologically relevant behavioural traits within populations.
[26] Raymond B. Huey and his colleagues used the same MA lines method, suggesting that mutation accumulation in Drosophila melanogaster significantly depresses only some behavioural traits.
Theory predicts that organisms can adjust the allocation of resources to male and female offspring in response to environmental conditions.
For example, female wasps can adjust their offspring sex ratios by choosing whether to fertilize an egg because they are haplodiploid.
Aggressive individuals can be better able to compete for resources including food, territory and mates, as well as more successful in protecting themselves and their progeny from predators.
For example, when individuals suffer from a mutation that causes them to have low levels of serotonin, there is an observed increase in impulsivity and depression[8] With neurotransmitters playing a central role in the development of aggressive behaviour, it follows that many of the gene mutations that have been implicated with aggressive behaviours are involved in the breakdown and/or receipt of neurotransmitters.
Alexis Edwards and her team identified 59 mutations in 57 genes that affected aggressive behaviour in Drosophila melanogaster.
Another contributor to the unequal male-female aggression ratio are the sex-linked gene mutations that affect only male behaviour, such as MAO-A mentioned above.
Other evolutionary and genetic explanations of violent behaviour include: dopamine receptors mutations, DRD2 and DRD4,[8] that, when mutate simultaneously, are hypothesized to cause personality disorders, low serotonin levels increasing irritability and gloom[30] and the effects of testosterone[32] on neurotransmitter functioning to explain the increased occurrence of aggression in males.