Genes can encourage children on bullying?

When and how often do you think your actions and behaviour are affected by your genes?

When and how often do you think your actions and behaviour are affected by your genes?
Many studies have been conducted that has proven that genes are the cause of various changes in appearance and behaviour. However in many cases, there are conflicts based on whether behaviour is a cause of “Nature or Nurture”.

It has been known that the environment that the children were brought up in is a major determinant of their behaviour. On the other hand, there was some research provided to suggest that ‘bullying’ is another trait that genes can express. At the University of Virginia in US, Paige Harden and colleagues have found that the cause bullying in children might also be inherited from the genes. Their study involved reviewing children born as twins; whether they had antisocial behaviours after witnessing their parents fight. The results were that they found that there was high percentage of twins having antisocial behaviour regardless of the witnessing of their parents’ fight even when their cousin (who shares similar genes) showed antisocial behaviour.

Since there are many other factors involved in the review, there is no definite answer to prove that genes are the cause of bullying behaviour in children. However, the study proved that witnessing of their parents’ fight is irrelevant to their behaviour.

Original article: http://www.newscientist.com/article/dn11125-genes-may-be-underestimated-cause-of-bullying.html

Min Young Kang

"Those Genes Suit Your Complection!"

by Lauren Smith (41741801)

With the incredible resources now available for mapping entire genomes comes the huge task of linking genotype to phenotype. Human skin pigmentation is one such area currently being investigated.

Skin Colour is determined by a combination of the thickness of one's skin and its level of melanin; the thicker one's skin, the 'yellower' it's pigmentation and the higher one's level of melanin, the darker one's skin.

Recent studies have identified specific single nucleotide polymorphisms (SNPs)which are genetic markers that impact the melanin biosynthesis pathway or melanosome biogenesis and hence skin pigmentation.

Such SNPs have been identified in the following genes:

TYR, TYRP1, OCA2, SLC45A2, SLC24A5
SLC24A4, IRF4, TPCN2, MC1R, ASIP, KITLG

This research has applications in fields ranging from the history of human evolution to treatment for albinos (humans with no melanin).

These findings are just a fragment of the slowly mounting evidence that Geneticists are beginning to understand the code which is the very language of life - DNA.

Reference list:
Sturm, R A (2009)Molecular Genetics of Human Pigmentation Diversity
US national Library of Medicine; http://www.ncbi.nlm.nih.gov

To find out more:

http://www.ncbi.nlm.nih.gov/pubmed/19297406?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_Discovery_RA&linkpos=5&log$=relatedreviews&logdbfrom=pubmed

http://www.biosci.ohio-state.edu/~pfuerst/courses/eeobmg640/reading2skincolor.pdf

Related Articles of Interest:

http://www.marieclaire.com/world-reports/news/latest/black-white-skin

http://www.msnbc.msn.com/id/28471626/

Eat a plant, become photosynthetic!

Elysia chlorotica, pictured right, is a green sea slug that lives along the Atlantic coastline of the United States. What makes this slug so unique is that it is able to ingest a certain species of algae (called Vaucheria litorea), store the algae's chloroplasts in the cells lining its gut, then run on "solar power" (i.e. convert sunlight into energy) for much of its life. Plant? Animal? Or freak?

The very fact that this slug can photosynthesise from ingested chloroplasts is perplexing; you see, the chloroplasts themselves contain only enough DNA to encode for about 10% of the proteins required for photosynthesis. Rumpho and her team hypothesised that the sea slug incorporates some of the algal DNA into its own DNA in a process called kleptoplasty. It is still, however, unclear as to how this occurs, but one theory is that some algal DNA is absorbed, along with the plastids, in the slug's gut.

Rumpho and her colleagues first sequenced the plastid genome of Vaucheria litorea and confirmed that it lacks the full complement of genes needed for photosynthesis. Then, to demonstrate the fact that the predator does indeed incorporate algal DNA into its own DNA, they showed that the nuclear gene of oxygenic photosynthesis, psbO, is expressed in the nuclear DNA of the sea slug. Furthermore, it was revealed that the psbO of the V. litorea is identical to that of the E. chlorotica, but absent in the mitochondrial genome of the latter organism.

The researchers believe that many more photosynthetic genes are absorbed by the sea slug through its diet, but do not completely understand as to how such plant genes are activated within the animal's cells.

Original article:

New Scientist - Solar-powered sea slug harnesses stolen plant genes

Additional information:

PNAS - Horizontal gene transfer of the algal nuclear gene psbO to the photosynthetic sea slug Elysia chlorotica

Author:

Insoo Kim (42050911), BIOL1020 P2

I'm seeing colour. (Beatrice Sim)

“I crashed the flight simulator because I started to hear with my eyes.” (5) It’s not one of the most conventional introduction lines that you’ll ever hear. But really, as many as 1% of the population actually has this form of synaesthesia; that is, auditory-visual synaesthesia. This neurological condition is characterised by the mixing of senses. This is caused by the crossing of sensory stimuli and the resulting combinations formed. For example, people with synaesthesia may see music – usually in the form of a colour – instead of just hearing it. The picture on the left is an example of how someone with synthaesthesia might view letters and colours.

It has been noted since the first description of synaesthesia, by Sir Francis Galton, that this condition tends to run in families, suggesting a genetic link. In fact, “40% of synaesthetes (sufferers of synaesthesia) have a first-degree relative.”(2) This, coupled with the fact that females seem statistically more likely to inherit this disease than males(1), has long since suggested to researchers that synaesthesia is linked to the X chromosome.

However, a recent study headed by Dr. Julien Asher (Department of Genomic Medicine, Imperial College, London), in collaboration with Professor Simon Baren-Cohen (Department of Psychiatry, University of Cambridge), indicates that this may not be the case. Using a “genome wide screen to search for susceptibility genes linked to auditory-visual synaesthesia”(1), they managed to identify four regions that could be linked to synaesthesia: on chromosomes 2, 5, 6 and 12. This suggests that the condition is multigenic. There was no evidence to suggest X-linkage.

Interestingly, the region on chromosome 2, which is most strongly linked to synaesthesia, has also previously been linked to autism. While this does not mean that the two conditions are related, it does suggest that this gene is “involved in how the brain gets built” [Hubbard 2009](3) In addition, the region on chromosome 6 is also linked to dyslexia.

All scientists involved are extremely optimistic that this identification of the genetic factors involved in this condition will be extremely useful. “Once we start to identify genes that are involved, we can start to look at what function they play in a mouse or monkey brain," he said, and then "come up with ways of studying what they do experimentally" Hubbard, a cognitive neuroscientist at Vanderbilt University in Tennessee said.

1 Science Daily 2009, Seeing Sounds or Hearing Colours: Scientists Narrow Search For Genes Associated With Synaesthesia, accessed 26 March 2009, http://www.sciencedaily.com/releases/2009/02/090205133728.htm.
2 Science Blogs LLC 2009, The Genetics of Synaesthesia, accessed 26 March 2009, http://scienceblogs.com/neurophilosophy/2009/02/synaesthesia_the_neurological_condition_in.php.
3 The Genes That Turn ‘Three’ Red 2009, American Scientist, accessed 26 March 2009, http://www.americanscientist.org/science/pub/the-genes-that-turn-three-red.
4 Synthesthesia 2009, Wikipedia Foundation, accessed 26 March 2009, http://en.wikipedia.org/wiki/Synaesthesia.
5 Egan, D. & Dick, L. 2007, 'The Right Stuff', House M.D., Fox, America.

Exercising in Genes

Whilst jeans and exercising may not work together, research into how our genes relate to our ability to exercise could prove very beneficial in understanding the human body. With obesity and many other exercise related health problems becoming more of an issue in today’s world, the need for exercise follows suit, and logically, so does research into how exercise works. It is known that some find it easier to lose weight than others and some are naturally more capable athletes than others. To support these observations scientists have so far identified a number of genes which affect our ability to ‘adapt to exercise.’

Adaptation to exercise simply refers to a person’s ability to improve in a particular area of exercise by repeating the exercise. If a person jogs every day, for example, then over time they will be able to jog faster and longer. This is because their body has adapted to the exercise. Dr. Olfert, of the University of California, examined the absence of an exercise related gene in mice. He found that mice without this gene were able to adapt to exercise more efficiently than mice with the gene.

Olfert also found that the gene FHL-1, affected a person’s ability to regulate their body’s glucose level. People who possessed one variant of the gene were able to avoid diabetes by exercising, whilst those with a different variant were not. Other research discovered that a person’s maximum oxygen intake was significantly affected by their genetics.

The problems encountered with this research are related to the great number of exercise related, and non-exercise related genes, and the complication of their combining effects. It could, however, contribute to a variety of scientific advancements in the near future. At the same time, it may also bring rise to even more ethical issues in the genetic engineering of animals and/or humans. For example, race horses and grey hounds with a genetically enhanced ability to adapt to exercise would likely be considered cheating; becoming a legal issue in the future, provided such advancements become applied commercially or illegally. Furthermore, applying this research on humans by altering particular genes could potentially cause unintended negative affects on the body. Regardless of this, research into how our genes affect our ability to adapt to exercise may provide further insight into the workings of our muscles and muscle-related diseases.


By 42017419


Sources:

Guilfoy, C 2009, Medical News Today, 19 March, viewed 22 March 2009, .

Images: http://images.teamsugar.com/files/users/1/12981/20_2007/get-physical-jog.jpg

APP - Causing and Protecting from Alzheimer's

Permanent changes and genetic mutations can cause diseases such as Alzheimer's. These genes can be inherited from parents.

I chose this topic as I find it amazing that scientists can pick the EXACT gene that causes such a dominant disease in our society. Anything that can help put a stop or help us control this, is more than welcome research.

There are two types of Alzheimer's Disease: early-onset and late-onset both of which have genetic links, however, the study of the APP gene is mostly on late-onset.

The new discovery of the APP gene has made some causes of late-onset Alzheimer's clearer.

Gene mutation on chromosomes which cause chromosome proteins is the major cause. APP makes the protein A-beta, which form together in the brain and block functions such as speech and memory leading to Alzheimer's.

In terms of heredity, if only one copy of the mutated APP gene is inherited from both parents, less A-beta proteins can form therefore making the occurrence of Alzheimer's Disease less likely; forming a sort of protection against the disease.

The discovery of this A-beta protein means that the conditions that occur in the 'one copy' brain can be mimicked using drugs. This means that the body can form its own 'protection' even if a person has two copies of the mutated gene.

Whether this treatment works or not, the discovery of the APP mutation changes the way Alzheimer's Disease is looked at even though it is known that even one copy of the gene is enough to cause the disease.

References:

1. http://kclmlc.files.wordpress.com/2008/02/dna_alzheimers.jpg

2. http://www.newscientist.com/article/dn16750-paradoxical-gene-causes-and-protects-against-alzheimers.html?full=true&print=true

3.http://www.nia.nih.gov/Alzheimers/Publications/geneticsfs.htm

4. http://www.topnews.in/health/files/alzheimers-brain.jpg4. 

Human Genes Required For Hepatitis C Viral Replication Identified

Although a few years away from being a possible therapeutic strategy, researchers from Massachusetts General Hospital (MGH) have made a startling discovery in the way they can block the reproduction of the hepatitis C virus (HCV).

Initial research to harness the replication of the hepatitis C virus related to the actual virus itself, with any form of treatment having a low success rate and often serious side effects that are intolerable for the patient. The new study reveals they can successfully block & suppress reproduction of the virus in cultured cells by targeting the genes that the virus utilises during its life cycle.

“For the current study the researchers examined whether blocking each of the approximately 21,000 predicted messenger RNA transcripts in the human genome with small interfering RNAs (siRNAs) had any effect on HCV replication.”

The results showed that 96 genes are associated with viral replication, from which they focused on several to conclude that blocking each of the particular genes, (one that focused on the coding of an enzyme called PI4KA, one that contributed to the formation of the COPI coat & one responsible for the regulation of the hepcidin protein), also blocked the HCV replication. Similar results were found when drugs were used to restrain the enzyme PI4KA & COPI.

Such research is vital as hepatitis C infects close to 200 million people worldwide & long-term infection can often lead to liver failure & liver cancer.

Such study is being attempted for other viruses including influenza, West Nile virus & HIV; one can only hope such progress is made.

"Now we need to work to uncover the molecular mechanisms by which these genes support HCV replication to get a better idea of which would be advantageous therapeutic targets," explains Raymond Chung, MD, director of Hepatology in the MGH Gastrointestinal Unit, the study's senior author.

s4175707

1. http://www.medicalnewstoday.com/articles/142921.php

2. http://harvardscience.harvard.edu/sites/default/files/full/hepCfull.jpg (IMAGE)

3. http://upload.wikimedia.org/wikipedia/commons/thumb/9/90/HCV_prevalence_1999.png/800px-HCV_prevalence_1999.png (image)

4. http://en.wikipedia.org/wiki/Hepatitis_C