AP Biology class blog for discussing current research in Biology

Author: naturalshalection

Scientist from China creates a baby resistant to HIV

The development of CRISPR technology has drastically progressed in the recent years, and He Jiankui, a scientist from China, took a step that most people judge to be crazy: he used CRISPR technology to create a human who is resistant to the HIV virus.

What is CRISPR? Good question.

CRISPR-Cas9 is a gene editing tool made from an ancient bacterial immune system. In bacteria, this system identifies DNA of invading viruses and send in different enzymes, such as Cas-9 to target and cut out a piece of DNA. Researchers quickly realized that almost any sequence of DNA can be cut out and modified the system to any sequence desired, even one that can prevent HIV. This is what Jianku’s work comprised of.

Jiankui and his team targeted the gene CCR5, a gene that provides the blueprint for the cell surface protein involved in the immune system, in the DNA of human embryos. The cell surface protein is usually involved in relaying information between cells, and HIV can use it to dock onto cells, infecting them with their own genetic material. Jianku eliminated the CCR5 gene to prevent HIV from docking onto any of the baby’s cells. However CRISPR-Cas9 induces mutations that scientist cannot fully control, and Jianku could not replicate the gene to the exact level. So, he instead created a “mixture of disrupted gene products”, which could potentially have a negative effect on human health.

At first glance, Jiankui’s experiment might be seen as beneficial, but Jiankui’s decision to create this human has been considered by other scientist as premature, drastic, and unethical, and has caused a lot of controversy. Although this was not the first time a scientist tampered with a human embryo, many scientists are outraged and believe that his experiment was a violation of human ethics. According to an article written by Allison Eck, the most notable ethical breach was conducting this experiment without the consent of other scientists, ethicists, regulators, or institutional review boards.

Debates over Jianku’s work have been circulating since the announcement of his experiment. Personally, I think that in the future, if we can prevent HIV and other harmful diseases that cause death, CRISPR can be an effective tool. However, as of now, we do not fully understand are aware of all of its effects. Therefore it is dangerous to test it on other humans. In the wrong hands, this powerful technology might be used in the wrong way and can cause huge repercussions. What do you think?


Plants Have Memory!

Did you know that flowering plants can remember changes in their environment? I sure didn’t!

Flowering plants use their memory to remember the temperature of a cold winter. By doing so, plants ensure that they will only flower during the warmer temperatures of spring or summer.

The way plants do this is through a group of proteins called polycomb repressive complex 2 (PRC2). In cold temperatures, the proteins come together as a complex and switch the plant into flowering mode. However little is known about how PRC2 senses the temperature changes in the environment.

But according to an article on Science News, a team of researchers from the Universities of Birmingham and Nottingham lead by Dr. Daniel Gibbs discovered a mechanism in angiosperms that enable them to sense and remember changes in the environment so they can adapt to the varying conditions around them, especially during the changing of seasons. The researchers discovered that the protein Vernalization 2 (VRN2), the core of the PRC2, is very unstable.

Why is this important? Since VRN2 is unstable, it can be greatly affected by the level of oxygen in the environment. In warmer months, the plant is already a flower, so it does not need to continue the flowering process. The abundance of oxygen causes VRN2 to break down. Conversely, when there is a lower level of oxygen in the colder months, VRN2 becomes more stable, causing the proteins of PRC2 to come together and switch the plant into flowering mode. As Dr. Gibbs says, “In this way, VRN2 directly senses and responds to signals from the environment, and the PRC2 remains inactive until required.”

By sensing and remembering the changes in their environment, plants can control their life cycle. I find it so interesting that plants have this capability. Plants that are able to adapt to our world’s ever-changing climate will be more successful in surviving.

Are microbiomes the real cause of arthritis?

It was thought that arthritis and joint pain afflicting obese people was caused by overstressed joints. However, an article from Genetic Engineering and Biotechnology News titled “Obese Microbiome May be the Real Cause of ‘Wear and Tear’ Arthritis” shows that the cause of arthritis is actually from inflammation driven by the microbiomes that live in the guts of obese people. The high-fat diet many obese people have unbalances the gut microbiome which in turn causes inflammation throughout their bodies, leading to very rapid joint deterioration. To solve the issue of arthritis, Micheal Zusick and his team at the University of Rochester Medical Center conducted an experiment on mice to see if a high-fat diet’s effects might be lessened with a prebiotic, a food that is high in fiber with the intention of improving the balance of microorganisms (in this case, microbiomes).


In a healthy mouse gut, Bifidobacteria , a beneficial probiotic bacteria, is abundant. Probiotics are live microorganisms intended to provide health benefits when consumed, generally by improving or restoring the gut bacteria. However when a mice becomes obese, proinflammatory species gain in abundance. In the first part of the experiment, Michael fed mice a high-fat diet, similar to a “cheeseburger and milkshake” human diet, and after only 12 weeks of this diet, the experimental mice became obese and diabetic. They doubled their body fat percentage compared to control mice, which were fed a low-fat, healthy diet. As predicted, the colons of the obese mice were dominated by proinflammatory bacteria, and almost completely lacked Bifidobacteria. The changes in the gut microbiomes of the mice were in conjunction with signs of inflammation, as when the researchers induced osteoarthritis (OA) with a meniscal tear, a common athletic injury known to cause osteoarthritis, OA progressed much more quickly in the obese mice than in lean mice, as nearly all of the obese mice’s cartilage disappeared within 12 weeks of the tear.

Micheal then repeated the experiment but this time gave the mice the prebiotic oligofructose. What do you think is going to happen?

The results showed that the effects of obesity on gut bacteria, inflammation, and OA were completely prevented when the high-fat diet of obese mice was supplemented with the prebiotic. Prebiotics cannot be digested by rodents or humans, but they are welcomed for certain types of beneficial gut bacteria, like Bifidobacteria because colonies of those bacteria chowed down and grew, taking over the guts of obese mice and crowding out bad actors, like pro-inflammatory bacteria. This, in turn, decreased systemic inflammation and slowed cartilage breakdown in the mice’s OA knees.

Oligofructose made the obese mice less diabetic but it did not change the mice’s body weight. Obese mice who were given oligofructose remained obese. They had the same load of weight on their joints yet their joints were healthier. Reducing inflammation was enough to protect joint cartilage from degeneration. This shows that inflammation is the cause of OA and joint degeneration.

I think this topic is very interesting because arthritis can be very painful and can change a person’s physical life dramatically. Helping people to minimize the stress on their joints could allow them to get up and do activities they couldn’t before, improving their quality of life.

Do humans have night vision?

Can humans see in the dark?

If you said yes, you are correct! When I saw the title of Emily Underwood’s article, “How humans- and other mammals- might have gotten their night vision“, it immediately intrigued me. Sight is an amazing gift that we all take for granted. Our eyes are incredible organs, and scientists are now discovering how they work when we see in the dark naturally. That is pretty cool!

Underwood’s article describes a study that gives insight into how our eyes work in the dark. According to her, “On a moonless night, the light that reaches Earth is a trillion–fold less than on a sunny day. Yet most mammals still see well enough to get around just fine—even without the special light-boosting membranes in the eyes of cats and other nocturnal animals.

In broad daylight, mammalian retinas respond to photons, which activate rods, which then send an electrical signal to the brain through a ganglion cell. It was thought that this retinal circuit was the same when the sun went down, but a new study by Greg Field and his colleagues at Duke University proves that the retinal cells adapt when there is no light to create what we know was natural night vision. How?

To understand this new study, we first need to know about direction-selective ganglion cells.

Direction-selective ganglion cells (DSGCs) specialize in motion detection. Depending on the movement of an object, different cells get excited. For example, some DSGCs fire when an object moves up and down and other DSGCs fire when an object moves from left to right. These ganglion cells play an important role in telling the brain where an object is moving towards. By doing this, the brain can make a decision as to how your body should act.

However, in the dark DSGCs behave very differently. Field’s experiments aimed to see how the DSGCs adapt when there is no light. His team examined slices of mouse retinas on glass plates embedded with electrode arrays. In an oxygenated solution, the mouse retinas could still “see” while the arrays recorded the electrical activity of the neurons. They ran the experiment twice: once under a normal “office light” setting, and once by dimming the lights to a moonlight setting. Looking at the results, Field found that three of the four directional DSGCs did not have a response to motion when they dimmed the lights. The only cells that were responding were the ones that usually respond to the motion “up” in daylight. In fact, these cells compensated for the other DSGCs, and were now responding to motions like “down” and “sideways”.

Why were the “up” DSGCs were acting differently? To answer this question, Field genetically engineered mice without intracellular gap junctions to run the experiment again. Gap junctions have previously been associated with night vision, and the results in Field’s experiment confirmed their relationship. The mice lacking gap junctions were not able to adapt to the dark. This shows that gap junctions are critical in boosting motion detection in the “up” cells when there is limited light.

It is still not known why specifically the “up” cells contribute to natural night vision, what do you think?

Field’s findings will be helpful to artificial vision efforts. DSGCs make up 4% of ganglion cells in humans, a small amount compared to 20% in mice. Yet a large part of retinal prosthetics relies on electrically stimulated ganglion cells. Studies like this can fine-tune the technologies that will be able to help visually impaired people, which is why I love reading about them. These experiments are crucial in progressing the future of medicine and the treatment of all kinds of health issues.

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