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Why does nature pass on genes?

pass-on-1pass-on-2

Selection is a directional process that leads to an increase or a decrease in the frequency of genes or genotypes. Selection is the process that increases the frequencies of plant resistance alleles in natural ecosystems through coevolution,  and it is the process that increases the frequencies of virulence alleles in agricultural ecosystems during boom and bust cycles.

How and when do typical genes contribute to fitness? A major puzzle: Most genes appear to be unnecessary!

Half or more can be “knocked out” (fully disabled) in yeast, worms, flies and even mice, without any obvious phenotypic effects (in the lab, anyway).

But these genes are maintained in evolution, so they must be useful. How? Two hypotheses:

  • (1) Most are “special-purpose” genes needed only under certain circumstances (stresses that occur in nature but not in the lab).
  • (2) Most are “fine-tuning” genes that increase the efficiency or accuracy of some physiological or developmental process in most environments.

Selection occurs in response to a specific environmental factor. It is a central topic of population and evolutionary biology. The consequence of natural selection on the genetic structure and evolution of organisms is complicated. Natural selection can decrease the genetic variation in populations of organisms by selecting for or against a specific gene or gene combination (leading to directional selection). It can increase the genetic variation in populations by selecting for or against several genes or gene combinations (leading to disruptive selection or balancing selection). Natural selection might lead to speciation through the accumulation of adaptive genetic differences among reproductively isolated populations. Selection can also prevent speciation by homogenizing the population genetic structure across all locations.

Selection in plant pathology is mainly considered in the framework of gene-for-gene coevolution. Plant pathologists often think in terms of Van der Plank and his concept of “stabilizing selection” that would operate against pathogen strains with unnecessary virulence. As we will see shortly, Van der Plank used the wrong term, as he was actually referring to directional selection against unneeded virulence alleles.

geno-dom-1

geno-dom-2

http://www.apsnet.org/edcenter/advanced/topics/PopGenetics/Pages/NaturalSelection.aspx

Click to access selection.pdf

selection

Your complete DNA sequence will help shape the future of medicine

Behaviour and genes

Jens Mowatt, I’m a brain that’s obsessed with brains.

Behaviour isn’t stored in genes, structure is. However, a different structure can lead to a different function of cells, and consequently a different behaviour by the organism.

In effect, your DNA just provides the building block for proteins. When an mRNA is transcribed from DNA, it is translated into a polypeptide that eventually is folded and converted into a functional protein. Once folded, the protein can function in processes within the cell, or it can be displayed on the membrane.

Humans are different from each other because our bodies make different proteins, and this makes our bodies function in a unique manner. For instance, a nepalese sherpa has a different haemoglobin gene than me, and this means his respiratory system is able to function more efficiently at high altitudes. It all starts at the cellular level.

Because genes lead to different structure and subsequently different functions in cells, they can also affect our behaviour. However, it isn’t as simple as that. The body is incredibly complicated. There are often countless genes involved in the same behaviour. There is almost never one gene determining a characteristic or behaviour.

If you wanted to genetically engineer an organism to make him/her more aggressive, you would probably have to change thousands of genes. You’d have to have knowledge about every single gene related to aggressive behaviour and know how to replace them with the correct alleles. It would be a pain in the ass. Its much easier to use artificial selection. When a criminal decides he wants to fight dogs, he wants the most aggressive ones so he can win fights. They select only the most aggressive dogs and breed them. This is essentially low-level genetic engineering. You’re selecting certain genes, specifically aggressive ones. The result is that you have offspring that are more aggressive. But this process often takes many generations, and can involve thousands of different genes.

Our behaviour is largely (or entirely) determined by the function of our brains. As such, the expression of proteins within the brain will determine the function of an organism. The polymorphisms in brain structure, neurons, glial cells and neurotransmitter/hormone levels are what will change the behaviour of an organism. There are many possible areas where different genes can lead to different behaviours. For instance, if an organism has a genetically different amygdala from most organisms, he will probably respond to stimuli in a different manner. Perhaps he has less of a fear response. Or, perhaps the organism’s anterior pituitary produces different levels of stress hormones, and this makes him respond to stress more acutely than other organisms of the same species. The possibilities are absolutely endless. They most certainly involve many different genes.

There may also be genetic difference in the amount (and distribution) of receptor proteins translated for neurons. Also, some people have naturally higher levels of neurotransmitters at certain synapses. For instance, some individuals have naturally lower baseline levels of dopamine in the mesolimbic system, whereas other people have higher baseline levels. The people with higher levels will respond more acutely to cocaine because it blocks reuptake of dopamine. As such, they need less cocaine to get the same effect as low baseline level people. The person will respond different to stimuli (i.e the drug) based on the set of genes expressed by his neurons. Do you see what I’m getting at here? There are countless areas where people can be genetically different in their brains.

One must always remember that there are often hundreds (if not thousands) of genes involved in a specific behaviour. You can’t say there is one gene for aggression, or one gene for peacefulness. Biology is incredible complicated. At our current level of knowledge, it isn’t that helpful to list a bunch of genes involved in a behaviour. Its often more helpful for neuroscientists to look at whole brain structures, or polymorphisms in brain receptors. In my opinion, reducing behaviours to a list of genes is a mistake.

There is too much of an emphasis on genes in our society. Too many people blame their genes for their behaviour; I think that is quite foolish. Genes play a large role in human behaviour, but you cannot ignore the effects of experience on the brain, and neither can you ignore epigenetic factors. We are greater than the sum of our genes.

https://www.quora.com/How-is-behaviour-stored-in-genes-Are-there-special-genes-for-special-behaviour
https://clubalthea.com/2016/10/14/your-complete-dna-sequence-will-help-shape-the-future-of-medicine/

Good genes when selecting a partner

good genes.JPG

Your complete DNA sequence will help shape the future of medicine

  • Orange and rust specks in the iris, can be prone to depression
  • Blue eyes. “Clinically speaking, people with blue or light-colored irises do tend to be more light-sensitive,” says Ruth Williams, MD, president-elect of the American Academy of Ophthalmology and an ophthalmologist at the Wheaton Eye Clinic in Chicago. “This is likely due to the sparsity of light-absorbing pigment in the eye.” The more pigment you have, the less light gets through the iris.
  • Gray, green, and blue eyes. Lighter-colored eyes may mean an increased risk for cancer. Because lighter eyes have less pigment to protect them from harmful ultraviolet rays, it’s true that light-eyed people have a greater lifetime risk for melanoma of the uvea, the middle layer of the eye, than their dark-eyed peers. “People with light iris color need to be diligent in wearing UV-protected sunglasses,” advises Dr. Williams. Melanoma of the uvea is an extremely rare cancer that affects the eye in about six of every million adults in the United States each year, and it is estimated that the incidence of the disease in black Americans, who are usually brown-eyed, is less than one-eighth the incidence in white Americans. In addition, although this is not directly related to vision, people with gray, green, or blue eyes tend to be fair-skinned and are at greater risk for skin cancers in general.
  • Brown eyes. A study done at the University of Louisville showed that people with brown eyes have slightly better reaction times when participating in certain athletic activities than light-eyed people. However, don’t use this small study to rationalize picking only brown-eyed people for your softball team. “In my experience, I couldn’t say we can judge performance based on eye color,” says optometrist Guadalupe Mejia, OD, of the University of Louisville.

Novel genetic mutations cause low metabolic rate and obesity

Researchers from the University of Cambridge have discovered a novel genetic cause of severe obesity which, although relatively rare, demonstrates for the first time that genes can reduce basal metabolic rate – how the body burns calories.

Previous studies (performed by David Powell and colleagues at Lexicon Pharmaceuticals in Texas) demonstrated that when the gene KSR2 (Kinase Suppressor of Ras 2) was deleted in mice, the animals became severely obese. As a result of this research, Professor Sadaf Farooqi from the University of Cambridge’s Wellcome Trust-MRC Institute of Metabolic Science decided to explore whether KSR2 mutations might also lead to obesity in humans.

In collaboration with Dr Ines Barroso’s team at the Wellcome Trust Sanger Institute, the researchers sequenced the DNA from over 2,000 severely obese patients and identified multiple mutations in the KSR2 gene. The research was published online today, 24 October, in the journal Cell.

Your complete DNA sequence will help shape the future of medicine

KSR2 belongs to a group of proteins called scaffolding proteins which play a critical role in ensuring that signals from hormones such as insulin are correctly processed by cells in the body to regulate how cells grow, divide and use energy. To investigate how KSR2 mutations might lead to obesity, Professor Farooqi’s team performed a series of experiments which showed that many of the mutations disrupt these cellular signals and, importantly, reduce the ability of cells to use glucose and fatty acids.

Patients who had the mutations in KSR2 had an increased drive to eat in childhood, but also a reduced metabolic rate, indicating that they have a reduced ability to use up all the energy that they consume. A slow metabolic rate can be found in people with an underactive thyroid gland, but in these patients thyroid blood tests were in the normal range – eliminating this as a possible explanation for their low metabolic rate. People have speculated for a long time that some individuals may burn calories more slowly than others. The findings in this study provide the first evidence that defects in a particular gene, KSR2, can affect a person’s metabolic rate and how their bodies processed calories.

Professor Farooqi said: “Up until now, the genes we have identified that control body weight have largely affected appetite. However, KSR2 is different in that it also plays a role in regulating how energy is used in the body. In the future, modulation of KSR2 may represent a useful therapeutic strategy for obesity and type 2 diabetes.”

Changes in diet and levels of physical activity underlie the recent increase in obesity in the UK and worldwide. However, there is a lot of variation in how much weight people gain. This variation between people is largely influenced by genetic factors, and many of the genes involved act in the brain. The discovery of a new obesity gene, KSR2, adds another level of complexity to the body’s mechanisms for regulating weight. The Cambridge team is continuing to study the genetic factors influencing obesity, findings which they hope to translate into beneficial therapies in the future.

http://www.cam.ac.uk/research/news/novel-genetic-mutations-cause-low-metabolic-rate-and-obesity

Your complete DNA sequence will help shape the future of medicine

Do obese people have a higher or lower metabolic rate?

fat

Several factors determine your basal metabolic rate:

  • Your body size and composition. If you weigh more or have more muscle mass, you will burn more calories, even at rest. So people who weigh more are more likely to have a faster metabolic rate — not a slower one — because a portion of excess weight is muscle tissue.
  • Your sex. If you’re a man, you probably have less body fat and more muscle mass than does a woman of the same age, so you burn more calories.
  • Your age. As you get older, your muscle mass decreases, which slows down the rate at which you burn calories.

Rather than slow metabolism, factors more likely to contribute to weight gain include:

  • Eating too many calories
  • Getting too little physical activity
  • Genetics and family history
  • Certain medications
  • Unhealthy habits, such as routinely not getting enough sleep

Your complete DNA sequence will help shape the future of medicine

From:

http://onlinelibrary.wiley.com/doi/10.1038/oby.2009.162/abstract

Gender was a significant determinant of BMR (basal metabolic rate) in children and adolescents but not in adults. Our results support the hypothesis that the age-related decline in BMR is due to a reduction in FFM (fat free mass). Finally, anthropometric predictors of BMR are as accurate as body composition estimated by BIA (tetrapolar bioelectrical impedance analysis).

Pyschological Management of Food Stressors is more important

The totality of energy expenditure is comprised of three main parameters: physical activity, the thermic effect of food (TEF), and resting metabolic rate or RMR [12]. Physical activity itself is comprised of both formal and nonexercise activity thermogenesis, termed “NEAT” [13]. These parameters have been estimated to constitute 30% (physical activity), 10% (diet induced thermogenesis), and 60% (RMR) of total daily energy expenditure. RMR is largely derived from the influence of “active tissue mass”, itself related to tissue oxygen usage [14]. Basal metabolic rate (BMR) is defined as the energy requirement necessary to maintain the function of cellular processes and differs from (is lower than) the resting metabolic rate, which constitutes the energy requirement to quietly rest while awake [1]. Nevertheless, an adult of normal body weight has a BMR/kg exceeding that of an obese adult by 1 to 1.5 times [15].

Obese subjects who have been energy restricted to induce weight loss display a rapid reduction in such active tissue mass with less of a reduction in metabolically less active tissue compared with controls [16]. These values however are subject to environmental modulation. Diet composition for instance is known to directly impact the TEF, with protein consumption inducing increased caloric expenditure manifested as heat production when compared with the other macronutrients [17, 18]. Not only has the TEF been shown to be an important contributor to satiety, with protein also being the most satiating, but the TEF is known to be higher in lean subject as opposed to their obese counterparts [19]. Thus, through such means, diet composition may play an important role in weight loss. Indeed studies have confirmed this conclusion [20, 21].

As described, one of the largest contributors to daily energy expenditure is RMR. With such a large influence upon energy expenditure, diet therapy aimed at modulating these effects may prove salutary. Specific dietary alterations amenable to positive changes in RMR may be more effectual than changes in TEF.

Genes and Cancer

How faulty genes lead to cancer

Our genes pick up mistakes that occur when cells divide. These mistakes are called faults or mutations and happen throughout our lives. They are caused by the natural processes in our cells, and by various other factors. These include

  • Tobacco smoke
  • Radiation
  • Ultraviolet radiation from the sun
  • Some substances in food
  • Chemicals in our environment

Sometimes people inherit certain faulty genes from their parents that mean they have an increased risk of cancer.

Your complete DNA sequence will help shape the future of medicine

Usually, cells can repair faults in their genes. If the damage is very bad, they may self destruct instead. Or the immune system may recognise them as abnormal and kill them. This helps to protect us from cancer.

faulty DNA.JPG

But sometimes mutations in important genes mean that a cell no longer understands its instructions, and starts to multiply out of control. It doesn’t repair itself properly, and it doesn’t die when it should. This can lead to cancer.

There are four main types of gene involved in cell division. Most tumours have faulty copies of more than one of these types.

Genes that encourage the cell to multiply (oncogenes)

Oncogenes are genes that, under normal circumstances, play a role in telling cells to start multiplying and dividing. Normally, in adults, this would not happen very often.

We can think of oncogenes as being a bit like the accelerator pedal in a car. When they are activated, they speed up a cell’s growth rate. When one becomes damaged it is like the accelerator becoming stuck down. That cell, and all the cells that grow from it, are permanently instructed to divide. So a cancer develops.

Genes that stop the cell multiplying (tumour suppressor genes)

Usually, cells can repair faults in their genes. If the damage is very bad, genes called tumour suppressor genes may stop the cell growing and dividing.

Mutations in tumour suppressor genes mean that a cell no longer understands the instruction to stop growing and starts to multiply out of control. This can lead to cancer.

The best known tumour suppressor gene is p53. The p53 gene is damaged or missing in most human cancers.

Genes that repair other damaged genes (DNA repair genes)

The DNA in every cell in our body is constantly in danger of being damaged.

But cells contain many different proteins whose job is to repair damaged DNA. Thanks to these, most DNA damage is repaired immediately, with no ill effects. But if the DNA damage occurs to a gene that makes a DNA repair protein, a cell has less ability to repair itself. So errors will build up in other genes over time and allow a cancer to form.

Scientists have found these genes to be damaged in some human cancers, including bowel cancer.

Genes that tell a cell to die (self destruction genes)

Some genes normally tell a cell to self destruct if it has become too old or damaged. This is called apoptosis or programmed cell death. It is a highly complex and very important process. Cells usually die whenever something goes wrong, to prevent a cancer forming.

There are many different genes and proteins involved in apoptosis. If these genes get damaged, a faulty cell can survive rather than die and it becomes cancerous.
Read more at http://www.cancerresearchuk.org/about-cancer/what-is-cancer/genes-dna-and-cancer#A6sK4pam5KWawIf3.99

Your complete DNA sequence will help shape the future of medicine

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