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Parental dominance in Imprinted Genes

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Parental dominance in Imprinted Genes

Introduction

Imprinted genes are a distinctive sub-set of genes that are expressed in one parental allele despite them having alleles from both parents. Parental dominance depends on whether allele is inherited from the mother or father. Paul (2014) notes that conception of a child is the start of a survival of the fittest struggle and this struggles continues all through the pregnancy.

 The parents’ DNA competes to control the baby and they both have different evolutionary goals. This battle for survival involves fetal genes that are already imprinted with molecules that had already marked them as coming the mother or the father. However, studies show that only 100 of the ten thousands genes are marked with this stamp (Davies, Dent & McNamara 28).  Research show that these genes as rare as they are they are critical for survival and if anything goes erroneous with the imprinting process during pregnancy it could to sickness of the fetus or even fatality of the mother or both.

Azim Surani who was a biologist working in the University of Cambridge laboratory was interested in a phenomenon that consisted of a healthy offspring being produced. The offspring would only contain the genes of the mother. This process was known as parthenogenesis.  This process was known only to occur in some invertebrates and also vertebrates such as fish, reptiles but was not to occur in mammals. This prompted Surani to try an experiment in the laboratory to test whether it would occur in mammals (Paul, 2014).

He used mice in his experiment. First he tried to inject genetic material from a female mouse into an egg but nothing happened.  The results were that some grew very slowly; other embryos were smaller than normal while others had a poorly organized brain tissue (Paul, 2014). Surani also attempted to do the same with male mice but the results also failed.

The conclusion to this experiment was that an offspring requires something essential from the mother and the father. The experiments did not fail because of genetic reasons but because of something that Surani could not explain at that time. Like there is sibling rivalry, an offspring tries to get most resources from both the mother and the father. David Hiag, a biologist suspected that competition for resources could give rise to the conflict between maternal and paternal genes (Killian, 2005).

. A good example is using the Kinship theory. This theory suggests that “males and females have a strong interest in seeing their offspring survive, but their reproductive strategies differ, leading them to want different things for their offspring” (Paul, 2014). Most female mammals are known to have more than one partner which prompts the male to have the interest to make sure that she uses all possible resources to develop his embryos (Davies, Dent & McNamara 30). The female on the hand have adapted to making sure that they have a maximum number of surviving offspring.

These offspring might have different father’s genes and they are all competing for her resources. The female has to come up with a strategy. She ensures that an embryo has just enough of what it needs and conserves the rest of the resources for the other offspring. This obviously created competition and this competition compromised of the imprints that were stamped on each of the fetus’s genes (University of Utah).

These molecular imprints could alter how the body reads the genetic code. This is because the genes can be turned on and off. There are two types of imprinted genes, those that are only inherited from the mother and those that are inherited from the father. The father’s interest in the offspring becoming larger than all the other offspring and therefore do anything possible to make sure this happens. Imprinted genes from the father would therefore encourage growth. This makes the embryo to demand more resources from the mother when it is in the womb (Davies, Dent & McNamara 31). The imprinted genes from the mother on the other hand encourage slow growth so that she can preserve the resources for the offspring that will follow.

There is an imprinted gene that is known as Igf2 gene which is responsible for the production of a protein that is responsible for growth and development of the fetus. Usually methyl tags silences the maternal Igf2 gene but if a DNA mutation occurs then it can lead to activating it again (University of Utah). This gene is only important for the growth of the embryo if it only comes from the father. This gene makes the embryo demand for resources from its mother. This only serves to prove that there is a struggle between the paternal and maternal genes as earlier theorized (Killian, 2005).

The strategy used by the father leaves the mother weak and can prevent her from getting other offspring. This is however not the case because the mother produces Igf2 receptors. This receptors stick on the protein and prevent it from circulating thus prevents it from encouraging more growth (Killian, 2005). The same way that the Igf2 genes work only when they are from the father, the Igf2 receptors work only when they come from the mothers. When the Igf2 is experimented in fathers the offspring becomes smaller than usual and when the Igf2 is knocked out in mothers the offspring becomes too big than the normal size.

Elizabeth Robertson was the first to discover an imprinted gene when she was experimenting on the roles that various genes play in the growth and development. As stated earlier when a gene that was switched off is activated it may have very bad effects on the offspring. According to Killian (2005), Beckwith-Wiedemann syndrome is a condition that is caused when imprinting goes wrong. This syndrome can occur when the Igf2 gene is turned on in both mother and father. The children that are born with this condition usually experience overgrowth. They are born larger than their peers and run the risk of having cancer especially in their childhood (University of Utah). If the father’s Igf2 is silenced then the child might be born underweight.

Imprinted genes can influence the behavior of an offspring through many ways. Loss of paternal or maternal genes may lead to Angelman (AS) or Prader-Will syndrome (PWS). When the paternal SNORD116 gene is lost it leads to PWS. PWS can occur when they are two maternal copies of the gene and which means that the paternal gene is missing. Children born with PWS show difficulty in learning, eating too much and is usually short than normal children. These children are also usually anxious at all times. MAGEL2 gene is also believed to be a contributor to the PWS. When the MAGEL2 gene is derived from the father, offspring show lack of proper feeding habits and also does not grow as expected (Dent & Isles 2013)

Errors that happen during imprinting in the genes that have control over the structure and the function ability of the brain have been known to cause mental illnesses. According to Dent & Isles (2013), patients with some of the disorders that are caused by imprinting of genes are known to have an extra large brain which makes them prone to autism. 

Imprinted genes are responsible for regulating the maternal supply and demand of nutrients. The imprinted genes in the mother ensure that the offspring have enough resources for the current offspring and that of the offspring to follow. Igf2 receptor helps the mother to prevent growth that has been induced by the male Igf2 (University of Utah). This helps the mother to properly regulate the resources that are being scrambled for by her offspring. Imprinted genes in mothers also help her to conserve nutrients for the offspring that are yet to come.

Imbalance of the Igf2 gene can lead to the abnormality of an offspring. Igf2 gene is only active when it comes from the fathers. If it comes from the mother or both parties, it might lead to the rise of an abnormal child (University of Utah). When Igf2 is activate in mothers the offspring suffers from Beckwith-Wiedemann syndrome. Imprinting of genes in the brain can also be affected by the environment that is around us. The post natal and prenatal environments can affect the imprinting of genes. This is because the brain is usually sensitive during these two periods. A mother’s diet during pregnancy and after birth has some hand in how the genes will be imprinted on the brain (University of Utah).  

Imprinted genes are under greater pressure of selection than the normal genes. This is because an offspring cannot have two imprinted genes at the same time. This results to imprinted genes evolving more quickly than all the genes. Imprinting usually happens when egg and the sperm are being formed. Therefore, it can be said that diet, hormones and even toxins can affect the process of imprinting of genes which in turn can have effects on the future generations.

Works Cited

Davies, Jennifer. Dent, Claire. McNamara, Grainne. Isles, Anthony.“Behavioral Effects of Imprinted Genes”.Current Opinion in Behavioral Sciences Vol. 2. pp 28-33.Web. 4 Aug. 2014. 29 Oct. 2014. <http://www.sciencedirect.com/science/article/pii/S2352154614000102>

Dent, Claire. Isles, Anthony. “Brain-expressed imprinted genes and adult behavior: the example of Nesp and Grb10”. Mammalian Genome Vol. 25, Issue 1-2. pp 87-93. Web. 24 Aug. 2013. 29 Oct. 2014. <http://link.springer.com/article/10.1007/s00335-013-9472-0>Weeners

Killian, Keith genomic imprinting : parental differentiation of the genome. Atlas Genet Cytogenet Oncol Haematol. (2005);9(4):347-361 Web July 2005 www.atlasgeneticsoncology.org/Deep/GenomimprintID20032.htl

Raeburn, Paul. “Genetic Battle of the Sexes”.Discovermagazine.com.23 May 2014. Web.29 Oct. 2014. <http://discovermagazine.com/2014/june/15-genetic-battle-of-the-sexes>

University of Utah. Genomic Imprinting. Retrieved from www.learn.genetics.utah.edu/content/epigenetics/imprinting/

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