Genetically Modified Cattle Show Resistance to Tuberculosis.

Research performed at Northwest A&F University in China produced the first genetically modified (GM) cattle resistant to tuberculosis.  The cattle produced were more difficult to infect and were largely protected against the actual symptoms of the disease. Myobacterium bovis is the bacteria responsible for bovine TB, which is a close relative to the bacteria that causes TB in humans. Bovine TB affects several species worldwide other than cattle and currently, the only methods of controlling the disease are culling or placing the animals on antibiotics, which can both be extremely costly and/or devastating. When one cow shows up positive for a TB test, usually the entire herd is culled to prevent possible other positives, and human transmission. In undeveloped regions, there is no effective control of the disease, and it can spread to humans via drinking an infected cow's unpasteurized milk.

The researchers deleted naturally occurring genes and inserted mouse gene SP110 into Holstein-Fresian cattle DNA using a technique called TALEN. In mice, SP110 helped protect them against TB transmission. 23 GM calves were produced. 13 calves lived into adulthood, and when their cells were studied, they showed higher resistance to M. bovis than cattle that were not genetically modified. The next step of the study was to introduce M. bovis into the lungs of 3 of the 13 GM cattle and 3 control (non-GM) cattle. Out of the GM cattle, 1 showed no signs of TB and the other 2 had reduced lesions on their major organs from the disease after necropsy several weeks later. Next, 9 of the 13 GM cattle and 9 control cattle were housed together with animals infected with TB. 6 out of the 9 GM cattle were not infected and the remaining 3 showed very minimal symptoms. All 9 of the control cattle contracted TB and had extensive lung damage.

While this study did not prove complete resistance, researchers say it is a goal to develop disease-resistant livestock.

GMO, antibiotics, culling... all of these things are huge in the animal welfare and nutrition world. While I personally do not have any issues eating GMO's, I am skeptical as to how this affects the future generations of cattle that have the SP110 gene. Just because the cattle are resistant to TB does not mean they are resistant to other diseases and infectious organisms either.

This is a HUGE step in the right direction, even if some find it morally displeasing. I think we need better methods at controlling transmission other than one gene for one disease at a time. There are still "mad cow disease", west nile virus, and other pathogens that can wipe out an entire herd. In my opinion, the bigger feat here is controlling transmission possibly via sanitation and appropriate farming methods. I applaud the scientists that were able to accomplish this study with goals they had expected, and hope that this helps in the future of zoonotic disease control.

Original Article: TALE nickase-mediated SP110 knockin endows cattle with increased resistance to tuberculosis

True Life: Honey I Shrunk the Kids

Or... the ants.

If carpenter ants weren't big enough, be prepared. Research performed at McGill University in Canada revealed that the Egfr gene (epidermal growth factor receptor) can affect surrounded genes into altering the sizes of the ants.

Naturally, the size of ants depends on their role in the colony. Obviously, the Queen is the largest. Differences in nutrition and chemicals determine what role an ant will have, and thus determines size. The chemicals directly affect different parts of genomes. Carpenter ants collected from Tallahassee, Florida were collected and brought back to the lab in Canada. Researchers at the University used a mechanism called "DNA methylation", which means that methyl groups (molecules) were added to certain DNA sequence sections. The ant larvae were exposed to drugs that increased or decreased the level of DNA methylation of the Egfr gene. The higher the methylation, the larger the ant size. The gene is indirectly regulated by DNA methylation, which can change the transcription of a gene completely, and thus change the size of an organism. Surrounding genes involved in cellular growth can also be altered due to the Egfr gene.

Researchers involved with this study hope that using these techniques, they can one day change how much a gene is expressed to even limit the growth of cancer and other disease cells.

While ants creep me out, I think this is fantastic news in epigenetics. In a lab setting, sizes of already living beings have been changed based on a physical process. They are larvae, already alive, being exposed to something that can alter their next phase of life. My only speculation with a tool like this is if it is used improperly. I would love to make a breakthrough in conquering cancers and other diseases by reducing their growth and possibly stopping growth altogether. However, I feel if we alter the sizes of animals, it can harm the environment if not controlled properly. Plenty of species have been introduced into unnatural habitats intentionally or unintentionally thanks to humans. Ants twice the size of what they are normally can ravage and destroy local colonies and thus upset the natural balance.  It's a battle the world is all too familiar with, but it is absolutely a possibility.

Original Article: Epigenetic variation in the ​Egfr gene generates quantitative variation in a complex trait in ants

Passing Silenced Genes

Using roundworms, geneticist Antony Jose and two graduate students were able to discover a new mechanism to pass silenced genes to offspring.  The silenced genes can stick around for as long as 25 generations, which can push evolution to occur at a more rapid rate.  It's also believed that this new mechanism can be used to treat genetic diseases.

The team caused the worm's nerve cells to produce double-stranded RNA (known as dsRNA) that matched specific genes of their DNA.  The dsRNA can travel between body cells, and even germ cells.  Once the dsRNA matches up with the correct section of DNA, the gene will be silenced.  By being able to travel into germ cells, the silenced gene is able to be included in gametes, encouraging the passage to offspring.  The team saw silenced genes present in up to 25 generations, showing that environmental triggers could potentially cause evolution to occur.

The team plans on doing more research to determine if this process happens in other species, including humans, which would allow for insight on the potential of evolution and the development of medications.  Being interested in the creation of medication, I believe that finding mechanisms that can be applied to treatment is amazing.  It's known that epigenetics plays a role in cancer as well; so discovering a mechanism that could potentially be involved in cancer is interesting to read about.

Primary Article 
Secondary Article

Mother's Diet and Child's Gene Expression

It has already been shown that the diet of female animals upon conception can have obvious effects on their offspring. For example, studies have shown that a female mouse's diet can permanently effect the coat color of her offspring. It has always been suspected that their must be similar correlations between a mothers diet and the genes of her offspring in humans. Researchers with MRC International Nutrition Group have shown that a human mother's diet can have significant effects on the "silencing" of her child's genes.

There is a strong dependence on the consumption of grown foods in Gambia. There is also distinct rainy and dry seasons which have extreme effects on the growth of these foods, meaning the diets of Gambia's people changes with the seasons. Researchers sampled 167 pregnant women (84 of which conceived at peak of rainy season and 83 conceived at peak of dry season) and tested nutrient levels in their blood as well as examining the genes of the child. It was found that those mothers who conceived at the peak of the dry season consistently had children with less methyl groups (which are used for the silencing of certain genes) than those who had conceived at the peak of the rainy season. The inability of silencing certain genes can have serious repercussions such as proneness to disease. Good nutrients at the time of conception is vital for gene expression and to help avoid some diseases. This is a revolutionary breakthrough in that scientists can now continue testing and begin on helping mothers to be to create prime diets for optimal methyl group production.

Article Link: http://www.sciencedaily.com/releases/2014/04/140429125733.htm
Related Article: http://www.genengnews.com/gen-news-highlights/mother-s-diet-has-life-long-effects-on-child-s-gene-function/81249809/

You Are What Your Mom Eats

In an article posted on the NewsMedical website, researchers from the U.S. Department of Agriculture (USDA) have made some remarkable discoveries that help explain how the diets of pregnant mothers in the days and weeks around the time of conception may affect genetic function in their children, and ultimately their children's health. Lead by molecular geneticist Robert A. Waterland, investigators examined the gene functions of 50 healthy children living in rural villages in the West African nation of The Gambia.

Specifically, Waterland was examining the effects of nutrition on what geneticists refer to as "epigenetic mechanisms" which impact the levels at which DNA methylation, occurs at regions of certain genes. Their studies revealed higher levels of DNA methylation at regions of five genes in children conceived during the peak rainy season months, when food would typically have been less available to mothers.

“We thought that peak rainy season hunger would lower levels of DNA methylation in children conceived at that time, but we found exactly the opposite. We don’t yet know why that happens, but we have more detailed studies under way that may give us the answer.”

Waterland stated that, two of the five elevated genes warrant further study because they are associated with risk of disorders such as Tourette's syndrome and hypothyroidism.

I struggle with Tourette's syndrome myself so this article was of particular interest to me. However, I do not think it had much to do with whether my mother conceived me during the rainy seasons in New Jersey. After reading this article, I am curious though as to whether or not her diet may have had any impact. I also have a hyperthyroid but here they are referring to hypothyroidism. Either way, both are closely related thyroid disorders.