Lunar LIGO and gravitational wave astronomy on the Moon

Gravitational wave astronomy continues to be one of the exploration concepts under consideration in NASA's strategy for conducting physics and astrophysics from the lunar surface. As with other proposals for new concepts in science and astronomy from the Moon, this one has a number of very interesting features which need to be developed further in order to assess them adequately. The possibility of robotic deployment of a gravitational wave antenna on the Moon in a triangular configuration and the question of closure on the third interferometer leg are discussed here

Lunar LIGO: A new concept in gravitational wave astronomy

For three decades, physicists have been in search of an elusive phenomenon predicted by Einstein's general theory of relativity; gravitational radiation. These weak vibrations of spacetime have, thus far, eluded conclusive Earth-based detection due in part to insufficient detector sensitivity and noise isolation. The detection of gravitational waves is crucial for two reasons. It would provide further evidence for the validity of Einstein's theory of relativity, the presently accepted theory of gravitation. Furthermore, the ability to identify the location of a source of a detected gravitational wave event would yield a radical new type of astronomy based on non-electromagnetic emissions. We continue our study of a lunar-based system which can provide an important complement to Earth-based analysis because it is completely independent of the geophysical sources of noise on Earth, while providing an Earth-Moon baseline for pin-pointing burst sources in the Universe. We also propose for the first time that a simplified version of the LIGO beam detector optical system, which we will call LLIGO (Lunar LIGO), could be emplaced on the Moon as part of NASA's robotic lander program now under study (Artemis). The Earth-based investigation has two major programs underway. Both involve large interferometer-type gravitational wave antennas

An oncogenic Ezh2 mutation induces tumors through global redistribution of histone 3 lysine 27 trimethylation

B-cell lymphoma and melanoma harbor recurrent mutations in the gene encoding the EZH2 histone methyltransferase, but the carcinogenic role of these mutations is unclear. Here we describe a mouse model in which the most common somatic EZH2 gain-of-function mutation (Y646F in human, Y641F in the mouse) can be conditionally expressed. Expression of Ezh2Y641F in mouse B-cells or melanocytes caused high-penetrance lymphoma or melanoma, respectively. Bcl2 overexpression or p53 loss, but not c-Myc overexpression, further accelerated lymphoma progression, and expression of mutant B-Raf but not mutant N-Ras further accelerated melanoma progression. Although expression of Ezh2Y641F increased abundance of global H3K27 trimethylation (H3K27me3), it also caused a widespread redistribution of this repressive mark, including a loss of H3K27me3 associated with increased transcription at many loci. These results suggest that Ezh2Y641F induces lymphoma and melanoma through a vast reorganization of chromatin structure inducing both repression and activation of polycomb-regulated loci