#micestudy – BioQuakes

Are you sick and tired of spending all of your time running on the treadmill and eating restrictive diets? Are you looking for a way to hack fat loss without ruining your way-of-life? Look no further than CRISPR gene-editing!

In humans, stubborn body fat can be attributed to either white or brown fat. Brown fat, specifically, is used in humans primarily for insulation, and can be tapped into when we are cold or need to ramp up our metabolism to generate heat. This fat is caused by a caloric surplus in humans, and is burned off by engaging in caloric deficit. However, in mice studies conducted by Steven Romanelli, Ormand MacDougald, and colleagues, CRISPR gene-editing offers promising results regarding the topic of brown fat loss in humans.

But what exactly is CRISPR gene-editing? CRISPR, or Clustered Regularly Interspaced Short Palindromic Repeat, gene-editing entails organizing short, palindromic DNA sequences of bacteria. These DNA sequences are surprisingly important in the immune function of these bacteria and other microorganisms, making CRISPR an incredibly promising and innovative tool in science research.

Bacteria have short sequences of variable DNA called “spacers” in between CRISPR DNA sequences. This DNA helps protect the bacterium from reinfection from viruses. If any virus were to attack the bacterium, the CRISPR DNA sequences would cut up that viral DNA matching any spacer within the genetic code of the bacterium, preventing it from reinfection.

CRISPR gene-editing works by processing invading viral DNA into short fragments that are inserted into the CRISPR DNA as spacers. Then, CRISPR replicates and spacers in the DNA of the bacterium experience transcription, in which DNA becomes RNA and CRISPR RNAs. These CRISPR RNAs help bacteria kill viruses, as they match the exact DNA as the viral DNA attacking the bacterium.

In mice experiments conducted by Romanelli, MacDougald, and colleagues, has used CRISPR gene-editing to have an enzyme named Cas9 break strands of DNA and a single piece of RNA to be packed into a harmless virus cell that will be delivered into cells in the study, which are brown fat cells in this case. This process has shown to delete several genes, namely the UCP1 gene in mice, that allows brown fat to exist and create heat. However, the mice in the study did not die when exposed to cold environments. They were able to survive despite a huge loss in brown fat.

Accordingly, using CRISPR gene-editing as a tool for brown fat loss in humans provides incredibly promising results. It is certain that, once CRISPR gene-editing becomes available for use in the reduction of brown fat in humans, I will no longer be using the treadmill as my mode of fat-burning and shift toward this method instead.

Stop Mice-ing Around Gene Editing in Mitochondria Is Now Possible

By samosome

On February 15, 2022

In Student Post

Mitochondria is often nicknamed the powerhouse of cells. It consists of a double membrane, DNA, ribosomes, inner membrane surface area fold called cristae, an inner fluid-filled space called the matrix. Mitochondria can self reproduce and can move around cells and change shape. It is also the site of cell respiration.

Structure of Mitochondrion

Mitochondrial DNA makes up only 0.1% of the human genome and is passed down exclusively from mother to child. There are around 1,000 copies of mitochondrial DNA in each cell. A cell is heteroplasmic if it contains a mixture of healthy and faulty mitochondrial DNA. If a cell has no healthy mitochondrial DNA, it is homoplasmic.

Mistakes in mitochondrial DNA affect how well the mitochondria work. Often more than 60% of the mitochondria in a cell will need to be damaged or mutated for mitochondrial diseases like mitochondrial diabetes to emerge. These diseases are often severe and, in some cases, fatal. They affect around every 1 in 5,000 people. These diseases are incurable and largely untreatable. Well until now….

The MRC Mitochondrial Biology Unit at the University of Cambridge found a possible answer in 2018. They used an experimental gene therapy treatment in mice. There they discovered that in heteroplasmic cells, they were successful in targeting and eliminating faulty mitochondrial DNA. Dr. Michal Minczuk shares that this new research does come with a catch, “It would only work in cells with enough healthy mitochondrial DNA to copy themselves and replace the faulty ones that had been removed. It would not work in cells whose entire mitochondria had faulty DNA.”

Pedro Silva-Pinheiro tells us, “This is the first time that anyone has been able to change DNA base pairs in mitochondria in a live animal. It shows that, in principle, we can go in and correct spelling mistakes in defective mitochondrial DNA, producing healthy mitochondria that allow the cells to function properly.” He, along with Dr. Minczuk and their other colleagues, have also used a biological tool known as a mitochondrial base editor. They use this to edit the mitochondrial DNA of live mice. The treatment works by it being delivered into the mouse’s bloodstream using a modified virus. It is then taken in by its cells. The editor looks for unique combinations of the A, C, G, and T molecules that make up DNA. Next changes the DNA base, changing a C to a T. Mitochondrial base editor can correct inevitable ‘spelling mistakes’ that cause the mitochondria to malfunction.

A recent example of how this research had been used is mitochondrial replacement therapy, or other known as three-person IVF. Mitochondrial replacement therapy replaces a mother’s defective mitochondria with a healthy donor’s. However, this process is extraordinarily complex and happens in fewer than one in three cycles in standard IVF.

The Impact of Newfound Generalized Taste Buds in Mice

By mydroxyl

On October 19, 2020

In Student Post

Background Information on Taste buds

According to this article about how taste buds work, taste buds are composed of cells that are structural, and cells that are chemical receptors. The surfaces of the receptor cells have proteins that bind with the chemicals that cause our perception of taste. As you all (should) know, the tongue does not actually have different sections for each flavor but instead, it has many different types of receptors that are stimulated by certain chemicals in food. The different reactions of receptors, which recognize bitter, sweet, sour, and umami flavors, are determined by specific genes in the DNA (It’s important to take note that the production of certain proteins and certain sequences of the DNA will even affect something as “simple” as taste). The receptor for salt, aka the epithelial sodium channel, functions differently from these receptors. It is basically a membrane that allows ions of sodium to permeate into specific cells.

The Mouse Research

An article (source article) from sciencenews.org reveals the findings of a research project that resulted in the discovery of generalized taste buds in mice that have the ability to taste four of the five flavors that these cells can recognize. These flavors include bitter, sweet, sour, and umami. The traditional belief in taste bud functionality is that taste buds only sense one or two specific flavors. Although mice possess both types of taste buds, the new research shows that clearly, the process is not as simple as just sensing specific tastes. Another article from sciencenews.org explains an experiment that demonstrates how taste is not just dependent on the taste buds themselves, but the brain plays a significant role in taste reception. In this experiment, certain receptors in the brains of mice were stimulated while the mice were drinking normal water. This caused the mice to react as if they were tasting sweet or bitter substances. The results of this experiment show that taste buds work with the brain to stimulate the perception of flavor.

This mouse is currently eating, meaning that its taste buds are currently sending signals to the brain to stimulate the perception of flavor.

Going back to the first article, mice need a specific protein that allows the generalized taste bud to send signals to the brain. Through research, it was discovered that the taste buds with broader ranges did not function in the absence of this specific protein. This goes to show the many functions and the vast significance of proteins in organisms. Additionally, some of the taste buds that only sense specific flavors were not functioning as well. Due to this, researchers believe that these two different types of taste buds depend upon each other to send signals to the brain.

So What?

At this point, you may be wondering why certain functions of the taste buds of mice matter. In case you didn’t know, the taste buds of mice function similarly to those of humans. This means that further research on the taste buds of mice may contribute to human interests as well. For example, one’s sense of taste can be lost through certain treatments (ex: chemotherapy) and aging. This may potentially lead to loss of appetite, causing malnourishment and other issues. With more research, these conditions could be treated through artificial taste bud receptors and even more by understanding the relationship between taste buds and the brain. Personally, I believe that this research is good support for those who are struggling with the loss of appetite, as well as a gateway to even more possibilities. I’d like to know more about your thoughts on this research. Is it worth the time and effort to learn more about this topic? Do you think that there are more possibilities than just treating loss of appetite? What else could this research be useful for?

BioQuakes

AP Biology class blog for discussing current research in Biology

Tag: #micestudy

Away With Treadmills and Low Carb Diets: Is CRISPR the New Hack For Fat Loss?

Stop Mice-ing Around Gene Editing in Mitochondria Is Now Possible

The Impact of Newfound Generalized Taste Buds in Mice

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