Danielle Henry

Long quiescent, stable and reproducible cylindrical plasma columns can be obtained as a result of the propagation of electromagnetic surface waves. The frequency of these waves is of the order of the electron-plasma frequency and it lies in that part (≃ 300-4 000 MHz) of the microwave spectrum where power generators with large enough output powers are readily available, at reasonable cost. Moreover, these waves can be excited very efficiently by using appropriate launching structures such as the surfatron. Such plasmas can, in certain instances, advantageously replace the positive column of DC discharges. This paper reviews the properties of the plasma columns sustained by the azimuthally symmetric surface wave. Special attention is given to the radial and axial electron density distributions, as well as to the radial density distributions of excited (radiative and metastable) atoms. Some demonstrated applications as well as further potential applications are also presented.

Telomere erosion in cells with insufficient levels of the telomerase reverse transcriptase (TERT), contributes to age-associated tissue dysfunction and senescence, and p53 plays a crucial role in this response. We undertook a genome-wide CRISPR screen to identify gene deletions that sensitized p53-positive human cells to telomerase inhibition. We uncovered a previously unannotated gene, C16ORF72, which we term Telomere Attrition and p53 Response 1 (TAPR1), that exhibited a synthetic-sick relationship with TERT loss. A subsequent genome-wide CRISPR screen in TAPR1-disrupted cells reciprocally identified TERT as a sensitizing gene deletion. Cells lacking TAPR1 or TERT possessed elevated p53 levels and transcriptional signatures consistent with p53 upregulation. The elevated p53 response in TERT- or TAPR1-deficient cells was exacerbated by treatment with the MDM2 inhibitor and p53 stabilizer nutlin-3a and coincided with a further reduction in cell fitness. Importantly, the sensitivity to treatment with nutlin-3a in TERT- or TAPR1-deficient cells was rescued by loss of p53. These data suggest that TAPR1 buffers against the deleterious consequences of telomere erosion or DNA damage by constraining p53. These findings identify C16ORF72/TAPR1 as new regulator at the nexus of telomere integrity and p53 regulation.