Effects and Correction of Atmospheric Pressure Loading Deformation on GNSS Reference Stations in Mainland China

Atmospheric pressure loading (APL) deformation is one component of nontectonic deformation for Global Navigation Satellite System (GNSS) time series and is a kind of deformation response caused by a redistribution of atmospheric pressure. In this paper, we present an atmospheric data processing strategy to compute the APL based on a spherical harmonic expansion of the global atmosphere pressure changes. We also provide a sample model to describe the relativity between the global atmosphere pressure changes and APL vertical deformation. The results show that the variation of air mass has a major impact on the north-eastern area of East China, the eastern area of North China, and Northeast China, and the vertical crustal displacement caused by the atmosphere changes in these regions can reach about 20 mm. The correction of APL for vertical time series of GNSS reference stations in different regions indicates that the arid area of the Northwest China, Northeast China, Central China, and North China are greatly affected by APL. While for the station located in Sichuan-Yunnan region, the amplitude and period change are small after correction of APL for vertical time series of GNSS reference stations, which reveals that the area is seriously affected by tectonic movement and water migration loading. The correlation between atmospheric pressure changes and crustal deformation is analyzed, which shows that APL has a serious impact on the north-eastern area of North China, the Northeast China, and the eastern area of Central China when the variations in atmospheric pressure in mainland China are the same. The research results of this paper will provide some reference value for the study of crustal structural deformation and the establishment of geodetic datum

Redeployment of Myc and E2f1-3 drives Rb-deficient cell cycles

International audienceRobust mechanisms to control cell proliferation have evolved to maintain the integrity of organ architecture. Here, we investigated how two critical proliferative pathways, Myc and E2f, are integrated to control cell cycles in normal and Rb-deficient cells using a murine intestinal model. We show that Myc and E2f1–3 have little impact on normal G1–S transitions. Instead, they synergistically control an S–G2 transcriptional program required for normal cell divisions and maintaining crypt–villus integrity. Surprisingly, Rb deficiency results in the Myc-dependent accumulation of E2f3 protein and chromatin repositioning of both Myc and E2f3, leading to the ‘super activation’ of a G1–S transcriptional program, ectopic S phase entry and rampant cell proliferation. These findings reveal that Rb-deficient cells hijack and redeploy Myc and E2f3 from an S–G2 program essential for normal cell cycles to a G1–S program that re-engages ectopic cell cycles, exposing an unanticipated addiction of Rb-null cells on Myc