The First Step Towards De-Extinction

In a recent article, scientists have been experimenting with "woolly mice", to help with the progression of bringing back the woolly mammoth. Obviously a mouse and an elephant are nowhere close to being the same animal, but scientists have been altering mice genes to include genes of a woolly mammoth. Such as the gene to enhance hair growth, and the gene responsible for the golden color that mammoths had. Scientists acquired the specific genes they needed, from 121 mammoth and elephant samples. They managed to create 32 different woolly mice, all varying slightly in appearance. 

It will be many more years, until we might see the return of woolly mammoths. However we could see the return of the dodo bird much sooner, according to Beth Shapiro. She explains that it will be much easier to alter the genetics of an animal that comes from an egg, rather than an animal that requires a surrogate mother, like an elephant.

   

I thought that this article was very interesting, because it talks about the idea of de-extinction. I feel like for as long as I can remember, the idea of bringing back extinct animals was always so unobtainable. Now, with the creation of woolly mice, we see that this is not the case, and in the next couple of years, we might even start seeing the return of animals that have been extinct for many years.

Peptide targeting senescent cells restores stamina, fur, and kidney function in old mice

In this article researchers were able to design a peptide to target senescent cells in mice.  This resulted in a restoration of stamina, fur density, and improved kidney function in naturally aged mice and fast aging mice.  The peptide works by blocking a protein for senescence.  The interference results in cell apoptosis in staying younger longer.  This could possibly lead to anti-aging medication. In a couple of years the average human life expectancy could possibly be doubled.  It's an interesting concept to think about.

https://www.sciencedaily.com/releases/2017/03/170323141414.htm

http://www.sciencedirect.com/science/article/pii/S0092867417302465

A Genetic Mutation That Leads to Obesity

Leptin is a hormone that is produced by fat cells and involved in regulating body weight. The function of this hormone is to interact with certain areas of the brain that are involved in controlling hunger. The hypothalamus and brain stem are responsible for sending signals to the body to let it know when to stop eating. There is a small percentage of people who have a genetic mutation in their leptin gene which leads to over-eating and eventually obesity. This genetic mutation is classified as hyperleptinemia. Hyperleptinemia is a condition where there is an increase of leptin in the bloodstream. When the leptin levels are high in the body then it can lead to the development of leptin resistance. Leptin resistance is a result of increased leptin which causes fat cells to increase as well. Due to leptin resistance, the brain cannot recognize when fat cells are dramatically increasing so the body is not signaled when to stop eating which leads to obesity. The physiological causes behind the development of leptin resistance is not fully understood by most people.

Researchers have conducted an experiment involving mice to determine whether the increase of leptin in the bloodstream leads to the development of leptin resistance. The mice used in this experiment were ob/ob and wild-type. This experiment discussed the effects of how a high- fat diet impairs the sensitivity of leptin to the neurons in the hypothalamus. There was two models that were developed from this experiment. One model proposed that leptin resistance is caused by increased plasma leptin levels which leads to overstimulation of leptin receptors and activation of negative feedback loops. The second model proposed that the dietary fats are directly responsible for the development of leptin resistance. The results from the experiment showed that as the mice were fed a high- fat diet they gained significant weight over a short period of time and their ability to limit their food intake was reduced. This confirmed that the diet- induced mice were resistant to leptin even when it was injected directly into their brain. The data from the results supported that hyperleptinemia and excess leptin signaling is required in order for leptin resistance to develop. 


I think that it is important to understand the effects of leptin deficiency and leptin resistance in humans and mice, and how obesity is a resulting factor. Additionally, this experiment provided valuable information that can help people that suffer from hyperleptinemia understand how it is developed. Lastly, the findings from this experiment can be used to potentially prevent this genetic mutation from occurring.

Mice Allow for Replication of Painlessness Mutation

There is a rare genetic mutation that prevents affected people from feeling pain. People affected by this mutation are born without a functioning sodium pathway Nav1.7. A new study was done in order to replicate this mutation in order for use with chronic pain patients in the future. Mice were used in this study, and it was found that both mice and humans affected by the mutation produce more opioid peptides. In order to observe whether or not opioids were important for painlessness, they gave an opioid blocker, naxalone, to the affected subjects. They found that they were able to feel pain afterwards.

Pain medicine for chronic pain patients is usually long term and can have bad side effects. The study resulted in filing a patent for a combination of opioids and Nav1.7 blockers in order to manage pain for effectively. This study also reinforced the fact that transgenic mice are able to model the nervous system of humans in order to test ways to replicate mutations from humans.

These findings are going to be extremely important when trying to treat patients with chronic pain. It eliminates the need for modern day pain medication. Patients usually develop a tolerance and a dependence on these medications that can have long lasting side effects. People with the affected mutation seem to develop no tolerance to opioids even though their bodies create more than the average person. If the researchers are able to find the right combination of blockers and opioids, this could lead to a real solution for pain.

Original Article.

The Entire Y Chromosome can be Replaced by Two Y Genes for Assisted Reproduction in Mice

In a recent article, Monika A. Ward, an associate professor at the Institute for Biogenesis Research at the John A. Burns School of Medicine explains “Does this mean that the Y chromosome (or most of it) is no longer needed? Yes, given our current technological advances in assisted reproductive technologies.” Ward and her colleagues identified the minimum Y chromosome contribution that is required to create a healthy first generation mouse, that is able to reproduce a second generation on its own without more technological intervention. The Y chromosome contribution is limited to only two genes, the testis determinant factor Sry and the spermatogonial proliferation factor Eif2s3y. The team used transgenic male mice with only the two Y genes and harvested their immature spermatids and then fertilized the oocytes of female mice through a technique called round spermatid injection (ROSI). The developed embryos were then transferred into female mice and live offspring resulted. Even though assisted reproduction can successfully occur without the Y chromosome, it is incredibly vital for normal fertilization and other aspects of male reproduction.

Above is a female mouse that was produced from a male that lacked the Y chromosome, but had the two necessary Y genes; the female is pictured with her own litter 

Even though the results of this study are incredibly significant, they cannot be directly applied to male infertility cases in humans. The ROSI technique is still considered experimental because there are issues regarding the safety of injecting immature germ cells. However, in this era where reproductive technologies are becoming more and more common, the ROSI technique may offer hope to overcoming male infertility once it is perfected in the future. There is no way that the Y chromosome will become obsolete as a result of this research, the study simply proves that the Y chromosome is not the only way for viable offspring to be produced. 

Article about the study on Scientific American