Telomeres are part of chromosomes, and their study is inseparable from the development of molecular biology. Molecular biology related experiments have relatively high requirements for the hygienic environment of the laboratory, and the conditions of no nucleic acid contamination need to be met. PCR Clean, a nucleic acid contamination removal reagent produced by MB in Germany, and a spray nucleic acid contamination removal reagent can easily and efficiently remove DNA, nuclease and other contamination.
Telomerase is an enzyme that maintains telomeres at the ends of natural chromosomes. Telomerase** sex chromosome ends synthesize telomere repeats, allowing the shelter protein complex to bind and protect the ends from DNA damage responses. If telomerase adds telomeres to the broken DNA ends, then the genes located at the broken ends may be lost. Theoretically, it would be inhibited in double-strand breaks (DSBs), where the formation of new telomeres leads to terminal truncation.
Recently, researchers have developed a method to detect novel telomere formation in Cas9 or I-SCEI-induced DSBS in human cells.
The study was published in Science under the headline: "ATR blocks telomerase from converting DNA breaks into telomeres".
Telomerase adds telomere repeats to the DSBS, resulting in interstitial telomere repeat insertion or the formation of functional new telomeres with terminal deletion. The threat of telomerase to genome integrity is minimized by dysregulated telangiectasia and RAD3-associated (ATR) kinase signaling, which inhibits the role of telomerase in excised DSBS. In addition to acting on excised DSBS, telomerase utilizes the extruded strand in the Cas9 enzyme product complex as a primer for the formation of new telomeres.
Scientists believe that although the formation of new telomeres is detrimental in normal human cells, it may allow cancer cells to escape from the break-fusion-bridge cycle. Human telomerase can act on broken DNA ends, threatening the integrity of the genome. Studies have shown that this genomically unstable aspect of telomerase is avoided by the ATR kinase component of the DNA damage response.