Recent research has revealed how “jumping genes,” specifically a type called LINE-1 (Long Interspersed Nuclear Element 1), manage to integrate themselves into human DNA by hijacking cell division.
Here’s a breakdown of the key findings:

• LINE-1’s Nature: LINE-1 elements are a type of retrotransposon, meaning they copy themselves using an RNA intermediate, similar to how the HIV virus operates. They make up a significant portion, about 20%, of the human genome. While most “jumping genes” are silenced in our bodies, LINE-1 is still capable of actively copying and inserting itself into new locations.
• Exploiting Cell Division: The new study, published in Science Advances, shows that LINE-1 takes advantage of a critical phase during cell division. When a cell divides, its nuclear envelope (the membrane surrounding the DNA) temporarily breaks down. LINE-1 RNA, along with one of the proteins it encodes (ORF1p), forms clusters that bind tightly to the cellular DNA during this brief period.
• Insertion Mechanism: This binding allows LINE-1 to position itself to insert its newly synthesized DNA copy into the host genome before the nuclear envelope reforms after cell division. This “copy-and-paste” mechanism effectively rewrites parts of our DNA.
• Implications:
• Genome Evolution: The constant movement and insertion of LINE-1 elements are significant drivers of human genome evolution, contributing to its diversity and complexity over time.
• Disease: While some insertions might be benign, if LINE-1 randomly jumps into essential genes, it can cause various diseases, including neurological disorders, cancer, and age-related conditions. It can also trigger an immune response leading to inflammation.
• New Therapeutic Avenues: Understanding this mechanism provides crucial insights into how these genetic elements propagate. Researchers hope this knowledge could lead to the development of therapies to prevent LINE-1 replication in cases where it causes harm.
  This research highlights the dynamic nature of our genome and the continuous interplay between our own DNA and these ancient, viral-like elements that have become integral to our genetic makeup.

Viruses are master of hijacking the cells they infact

Viruses are masters of hijacking the cells they infect. To make more copies of themselves, they take over the host’s genetic machinery. In doing so, they often leave behind small traces in our DNA. These traces, known as transposable elements, are tiny pieces of genetic material that act a lot like viruses. They are even simpler in structure, but they also rely on the cell’s own tools to reproduce.

Over time, our bodies have learned to silence most of these foreign sequences. But not all of them are inactive. A few remain restless, earning the nickname “jumping genes” because they can still move around the genome. Among them, one stands out. It’s called LINE-1, short for long interspersed nuclear element 1, and it’s the only one still capable of copying and pasting itself entirely on its own.

LINE-1 works in a clever way. It first creates a copy of itself using RNA, the close chemical cousin of DNA. Then, that RNA is converted back into DNA and inserted into a new spot in the genome. This copy-and-paste process is similar to how the retrovirus HIV operates, which is why LINE-1 is known as a retrotransposon.

In this way, retrotransposons add code to the human genome every time they move, which explains why 500,000 LINE-1 repeats now represent a “staggering” 20 percent of the human genome. These repeats drive genome evolution, but can also cause neurological diseases, cancer, and aging when LINE-1 randomly jumps into essential genes, or triggers an immune response like a virus to cause inflammation.

Implications for Future Research and Therapeutics

The work also suggests that the LINE-1 condensate acts as a delivery vehicle to bring its RNA into proximity of the right sequences (rich in the DNA bases adenine and thymine) on DNA where the retrotransposon tends to insert, say the study authors. Packaged in its condensates, LINE-1 is thought to evade mechanisms that exclude large particles from the nucleus during mitosis as a cellular defense against viruses.

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