Thanks to shRNA lentiviral vectors which target promyelocytic leukemia (PML), the authors show PML depletion induces telomere damage, nuclear and chromosomal abnormalities, and senescence. This work provides a novel view of the physiologic function of PML, which participates in telomeres surveillance in normal cells.
The authors used a LentiCRISPR-sgTRF2-1 to knockdown TERF2. They observe an exacerbation of mitotic telomere deprotection which increases the ratio of cells that died during mitotic arrest and sensitized cancer cells to mitotic poisons. They propose a crisis pathway wherein chromosome fusions induce mitotic arrest, resulting in mitotic telomere deprotection and cell death, thereby eliminating precancerous cells from the population.
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Thanks to shRNA lentiviral vectors which target promyelocytic leukemia (PML), the authors show PML depletion induces telomere damage, nuclear and chromosomal abnormalities, and senescence. This work provides a novel view of the physiologic function of PML, which participates in telomeres surveillance in normal cells.
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