Science: Your Birth Is Not an Accident, but Created by Gene "Intentionally"!

What is man? Is life meaningful? Where will man go?

The famous British evolutionary biologist Richard Dawkins expressed his views in his book—Selfish Gene. He believed that life is the machine to survive created by genes. Humans are just the carrier of the genes and saving genes is our ultimate goal for existence. Life is short, but the gene is immortal.

Genes are selfish, because they can better survive in natural selection conditions by continuous evolving, never considering whether it is suitable for the host survival. Now, scientists find that the genes are selfish not only in natural selection level. For their own survival, some genes would destroy their own kind.

According to our knowledge, mammals need meiosis during the production of eggs. During meiosis, one set of chromosomes in oocytes goes into the polar body and is then degraded. The other set of chromosomes goes into the egg and is passed on to offspring. At the same time, according to classical Mendel's genetic law, the two sets of chromosomes should have the same opportunity to enter the oocyte with both 50%. 

Recently, Professor Michael Lampson from University of Pennsylvania and his team have shown for the first time that some selfish genes in mammalian oocytes undergo "cheating" behavior during meiosis. These genes, in order to be able to go into the egg and be passed to offspring, they will "actively perceive" their position in the oocyte. Once they find being "eliminated", they will actively cut off the connection with the spindle, requiring redistribution of the position, in order to increase their chances of entering the egg. The finding was published in the journal Science. 

chromosome

For example, it's like two people playing with a pair of stone scissors, and the one who won will have the chance to survive. The first time you win, but your opponent cheats, and urges to play again, without your consent. It's obvious that the selfish man has a better chance of living.

The discovery had to start from 2001. At the time, Dr. Carmen Sapienza and others concluded that the separation of chromosomes was not random when meiosis was performed in mammals. In other words, the chances of two sets of chromosomes entering eggs were not equal. There were always some chromosomes that had a greater chance of entering the egg during meiosis. But at that time they didn't know why. Until recently, a series of studies have shown that the phenomenon of nonrandom segregation of chromosomes in mammals during meiosis is closely related to centromere. In meiosis, the centromere competes fiercely for the right to survive.

Centromere is actually a DNA sequence on chromosome, which is composed of a large number of repetitive DNA fragments. It is the most abundant non-coding DNA in mammalian cells. In the process of oocyte meiosis, the centromere is connected with the spindle and mediates the separation of chromosomes.

In recent years, scientists have found that a large number of DNA mutations and base deletions are accumulated in DNA sequences on centromere. And they're evolving fast, making their DNA lengths longer and DNA repeats become more. At the same time, the longer the DNA sequence of centromere is and the more DNA repeats it contains, the more centromere proteins are combined. The centromere is called strong centromere, because it has a greater chance of entering the egg to survive. However, the specific mechanism is not clear. 

In order to identify the cause, Professor Lampson began the experiment.

By mixing mice with strong centromere and weak centromere, professor Lampson obtained mice that could produce both strong and weak centromeric oocytes simultaneously. Then, when the 23 meiotic processes involving both strong and weak centromeric oocytes were observed, professor Lampson was surprised to find that there were 21 oocytes, whose chromosomes were not randomly separated.

Specifically, in 23 oocytes, 21 oocytes contained a strong centromeric chromosome during meiosis. When it came to the polar body, it would actively cut off the connection with the spindle, and also cut off the connection between the weak centromere and the spindle. Then it redistributed the position of the two in the oocyte, and reconnected with the spindle again, which ultimately increased its own chances of entering the oocyte. 

So how does a strong centromere do this?

Professor Lampson discovered that the reason for this phenomenon was that there was a large amount of CDC42 proteins on the side of the mouse oocyte that was about to form the polar body and then to be degraded. The protein could make the microtubule link to the spindle and the centromere acidate so as to become fragile.

At the same time, strong centromere was very sensitive to tyrosine mediated by CDC42 protein. As a result, the connections between the centromere and the spindle became weaker near the polar body, while the weak centromere was almost completely unaffected by the CDC42 protein, and only followed the "fate" arrangement.

Therefore, when strong centromere found itself to be "eliminated", it would actively cut off the connection with the spindle, and forced the connection of corresponding weak centromere and the spindle to be cut off, and then to redistribute. So the strong centromere had a greater chance of survival.

chromosome

It is not clear why the centromere is more sensitive to the CDC42 protein. But admittedly, this is one of the tools that centromere, a selfish gene, has used for cheating.

In fact, scientists have long discovered that the most abundant genes (called selfish DNA) do not contain any biological function. Because their current function is to spread themselves everywhere, to ensure their survival. The centromere is actually the most abundant and widely distributed class of DNA. 

It also means that the most abundant genes in our body have always been "silent" to struggle for their own survival, and they are trying to preserve themselves in violation of the "fair" rules of the game. As for our existence, perhaps it is just “a little gift” from these genes for their better survival. So someday, when these genes find out that we're not fit for them to live, they may not hesitate to give up on us to find a better host.

Quick Inquiry
Blog List
Date:
-