There is a fierce genetic warfare in our cells, and the invading foreign DNA frequently attempts to destroy the human genetic blueprint. Now, UCSF researchers have discovered a new molecular mechanism by which cells protect their genes from intruders.
This mechanism is responsible for identifying and targeting foreign DNA and is called SCANR by researchers. The UCSF researchers discovered the SCANR mechanism in yeast. Since yeast and human cells are very similar, they believe that similar mechanisms may exist in the human body. Such a mechanism helps reduce human genetic diseases and deaths associated with them.
SCANR's goal is a small piece of DNA called a transposon. For some newborns, the transposon is a deadly threat. In simple bacteria to complex humans, transposons are widespread, and these transposons that enter the host genome originate from other species.
The organism's own genes are only copied once during cell division, but transposons (also known as jumping genes) are different. They will replicate multiple times and randomly insert into the host cell's DNA. If the transposon is inserted into an important gene, it will cause malfunction of the gene function, causing disease or birth defects. Just as the immune system can recognize foreign invaders, researchers led by Dr. UCSF Hiten Madhani discovered that the genetic mechanism in the nucleus uses SCANR to identify and target transposons. The research was published in the journal Cell on February 13.
"We know that some human genetic diseases are caused by movable genetic elements," Madhani said. "Now we have found that cells distinguish between" me "and" non-me "in one step of gene expression, thereby preventing the transposon from spreading." Forever genetic warfare In the evolution process, transposons frequently cross species boundaries and break through Into the host genome. Fast-evolving bacteria often use them to transmit antibiotic resistance.
Nearly half of the DNA in the human genome contains transposons, and this percentage will increase in generations after generations. This is because about 20% of transposon replication is not subject to DNA replication rules during cell division. Nevertheless, over time, most transposons become inactive during generational alternations and no longer become threats.
According to Madhani, professor of biochemistry and biophysics at UCSF, there are a large number of transposons in the human genome, and 99% of the lotus genome is derived from transposons. The lower organism salamander has the same number of genes as humans, but due to the transposon replication, its genome can be about forty times that of humans. For this reason, newt cells are also larger than human cells.
Barbara McClintock discovered the jumping gene in corn, Richard Roberts and Phillip Sharp found that the genes on the chromosome would be separated by introns, and Andrew Fire and Craig Mello discovered RNA interference. These are important discoveries that have won the Nobel Prize. Based on this, UCSF researchers have revealed the mechanism of SCANR and its target transposon in the yeast Cryptococcus neoformans. Studies have shown that when cell shearing devices encounter introns such as transposons, they stall. SCANR recognizes this fault and starts to synthesize the corresponding "small interference RNA" molecule, which is used to neutralize the RNA of the transposon.
"Scientists may find that many ways of differentially expressing genes in higher organisms are similar to intron splicing in the SCANR mechanism. Such a mechanism helps to identify foreign genes and resist them," Madhani said.
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