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A set of nearly NS-trending rifts developed in the Himalayan orogen and southern Tibet, which are the large-scale extensional structures formed under the continuous compression of the Indo-Eurasia continent, playing a significant role in revealing the post-collisional evolution of the Tibetan Plateau. Different predictions have been made on the spatiotemporal distribution of these rifts through the existing hypothesis models, constituting the key factors constraining the formation system of the rifts. In this study we synthesized previous studies on the initiation time of rifting, and further clarified the spatiotemporal trend. The analysis results showed that the rifting initiated progressively earlier westward, which is consistent with the evolution of post-collisional magmatism in the Lhasa Terrain. Moreover, combined with the geophysical observations, it is inferred that the geodynamic mechanism of the nearly NS-trending rifts accords closely with the hypothesis model concerning the eastward-propagating lateral detachment of the subducted Indian slab. The Indian slab detachment resulted in asynchronous gravitational potential energy gradients, which drove the lithosphere flow eastward and eventually caused the eastward development of the rifting.

Defining the northern margin of the Tibetan Plateau, the Altyn Tagh Fault system (ATFs)exerts a crucial role in accommodating intracontinental deformation during the India-Asiaconvergence. The North Altyn fault (NAF), demarcating the western boundary of the ATFs inthe Altun Shan region, was testified to exist a structural shift from sinistral along-strikeslipping to thrusting during the Cenozoic era. However, the exact timing of the shift remainsan issue to be refined. In this study, we conducted LA-ICP-MS based apatite fission trackdating at massifs of both the hanging wall and footwall along the NAF, to shed light on datingthe thrusting-related exhumation of the NAF. The results show that the hanging wall massifsof the NAF present a quasi-isothermal quiescence during the early Cenozoic, followedby a rapid cooling phase with mean cooling rate of 6.66 ± 0.72 ˚ C / Ma since∼15 Ma, resulting from accelerated exhumation which has been interpreted tomark intense vertical uplift of the NAF. Significantly younger age (∼5 Ma) buthigher rate (15.33 ± 2.10 ˚ C / Ma) of rapid-cooling event occurred at the footwallcompared to the hanging wall suggests a northward propagation of thrusting into theinterior Tarim basin. Combining previous studies, we attribute the structural shift ofthe NAF from along-strike slipping to thrusting to the Mid-Miocene kinematicreorganization of the ATFs, supporting to the two-stage evolution model of theAFTs that: (1) during ∼50-15 Ma, the NAF acted as a part of the Altyn Tagh faultexperiencing along-strike slipping, with the Altun Shan elevated north within bigrestraining-double-bends; and (2) after ∼15 Ma, the Altyn Tagh fault cut through thedouble-bends with significant thrusting along the NAF, circumscribing the presenttriangle-shaped Altun Shan featured with uplifting south beginning at ∼15 Ma. [ABSTRACT FROM AUTHOR]

Ubiquitin-specific protease 31 (USP31) is a member of deubiquitinase family that is involved in nuclear factor-κB activation and sarcomagenesis. However, little is known about posttranslational modification in the regulation of its activity and cervical cancer cell growth. In our study, we found that the Lys1264 residue of USP31 can be modified with an acetyl group by high-resolution mass spectrometry in HeLa cell line, and site-specific mutagenesis can significantly increase USP31 ubiquitin hydrolase activity and decrease the expression of p65. When being transfected with a plasmid expressing mutated USP31, the number of cancer cells was significantly decreased. We also observed that mutated USP31 could promote apoptosis but not cell cycle by flow cytometer analysis. Overexpression of mutated USP31 could reverse the effect in USP31 knockdown cell line. To further investigate its activity in tumorigenesis, deacetylase sirtuin 1 (Sirt1) was shown to interact with USP31 by co-immunoprecipitation and blocking the function of Sirt1 by knockdown or the inhibitor nicotinamide could increase the acetylation of USP31. When Lys1264 of USP31 mutated, Sirt1 could not remove its acetylation and alter the expression level of p65. Finally, inhibition or knockdown of Sirt1 suppressed USP31 activity in HeLa cell line, leading to cisplatin-induced apoptosis resistance. Therefore, acetylation at Lys1264 suppresses USP31 activity and plays a protective role in cancer cell growth. Our study contributes to understanding the mechanism of USP31 activity regulation and its role in tumorigenesis., (© The Author(s) 2021. Published by Oxford University Press on behalf of the Center for Excellence in Molecular Cell Science, Chinese Academy of Sciences. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)