Revisiting the mechanisms of mid-Tertiary uplift of the NE Tibetan Plateau.

Contrasting views exist on timing and mechanisms of Tertiary crustal uplift in the NE Tibetan Plateau based on different approaches, with many models attributing surface uplift to crustal shortening. We carry out a comprehensive investigation of mid-Tertiary stratigraphy, sedimentology, and volcanism in the West Qinling, Hoh Xil and Qaidam basin, and the results challenge previous views. It was held that the discordance between Oligocene and Miocene strata is an angular unconformity in the West Qinling, but our field observations show that it is actually a disconformity, indicative of vertical crustal uplifting rather than crustal shortening at the Oligocene to Miocene transition. Widespread occurrence of synsedimentary normal faults in mid-Tertiary successions implicates supracrustal stretching. Miocene potassic-ultrapassic and mafic-ultramafic volcanics in the Hoh Xil and West Qinling suggest a crucial role of deep thermomechanical processes in generating crust- and mantle-sourced magmatism. Also noticeable are the continuity of mid-Tertiary successions and absence of volcanics in the Qaidam basin. Based on a holistic assessment of stratigraphic-sedimentary processes, volcanic petrogenesis, and spatial variations of lithospheric thicknesses, we speculate that small-sale mantle convection might have been operating beneath northeast Tibet in the mid-Tertiary. It is assumed that northward asthenospheric flow was impeded by thicker cratonic lithosphere of the Qaidam and Alxa blocks, thereby leading to edge convection. The edge-driven convection could bring about surface uplift, induce supracrustal stretching, and trigger vigorous volcanism in the Hoh Xil and West Qinling in the mid-Tertiary period. This mechanism satisfactorily explains many key geologic phenomena that are hardly reconciled by previous models.

Cretaceous basin evolution in northeast Asia: tectonic responses to the paleo-Pacific plate subduction.

Cretaceous rift basin evolution was an important part of the tectonic history of northeast Asia in the late Mesozoic. Three types of rift basins are identified-active, passive and wide rift basins-and they developed in different regions. Passive rift basins in the eastern North China craton are thought to be the consequence of crustal stretching and passive asthenospheric upwelling. Wide rift basins in the eastern Central Asian orogen are assumed to originate from gravitational collapse of the thickened and heated orogenic crust. Active rift basins in the northern North China craton are attributed to uprising of asthenospheric materials along a lithospheric-scale tear fault. Slab tearing of the subducting paleo-Pacific plate is postulated and well explains the spatial distribution of different types of rift basins and the eastward shifting of magmatism in the northern North China craton. The Late Cretaceous witnessed a period of mild deformation and weak magmatism, which was possibly due to kinematic variation of the paleo-Pacific plate.

PRC2 and EHMT1 regulate H3K27me2 and H3K27me3 establishment across the zygote genome.

The formation of zygote is the beginning of mammalian life, and dynamic epigenetic modifications are essential for mammalian normal development. H3K27 di-methylation (H3K27me2) and H3K27 tri-methylation (H3K27me3) are marks of facultative heterochromatin which maintains transcriptional repression established during early development in many eukaryotes. However, the mechanism underlying establishment and regulation of epigenetic asymmetry in the zygote remains obscure. Here we show that maternal EZH2 is required for the establishment of H3K27me3 in mouse zygotes. However, combined immunostaining with ULI-NChIP-seq (ultra-low-input micrococcal nuclease-based native ChIP-seq) shows that EZH1 could partially safeguard the role of EZH2 in the formation of H3K27me2. Meanwhile, we identify that EHMT1 is involved in the establishment of H3K27me2, and that H3K27me2 might be an essential prerequisite for the following de novo H3K27me3 modification on the male pronucleus. In this work, we clarify the establishment and regulatory mechanisms of H3K27me2 and H3K27me3 in mouse zygotes.

Deletion of BAF250a affects oocyte epigenetic modifications and embryonic development.

BRG1-associated factor 250a (BAF250a) is a component of the SWI/SNF adenosine triphosphate-dependent chromatin remodeling complex, which has been shown to control chromatin structure and transcription. BAF250a was reported to be a key component of the gene regulatory machinery in embryonic stem cells controlling self-renewal, differentiation, and cell lineage decisions. Here we constructed Baf250aF/F ;Gdf9-cre (Baf250aCKO ) mice to specifically delete BAF250a in oocytes to investigate the role of maternal BAF250a in female germ cells and embryo development. Our results showed that BAF250a deletion did not affect folliculogenesis, ovulation, and fertilization, but it caused late embryonic death. RNA sequencing analysis showed that the expression of genes involved in cell proliferation and differentiation, tissue morphogenesis, histone modification, and nucleosome remodeling were perturbed in Baf250aCKO MII oocytes. We showed that covalent histone modifications such as H3K27me3 and H3K27ac were also significantly affected in oocytes, which may reduce oocyte quality and lead to birth defects. In addition, the DNA methylation level of Igf2r, Snrpn, and Peg3 differentially methylated regions was decreased in Baf250aCKO oocytes. Quantitative real-time polymerase chain reaction analysis showed that the relative messenger RNA (mRNA) expression levels of Igf2r and Snrpn were significantly increased. The mRNA expression level of Dnmt1, Dnmt3a, Dnmt3l, and Uhrf1 was decreased, and the protein expression in these genes was also reduced, which might be the cause for impaired imprinting establishment. In conclusion, our results demonstrate that BAF250a plays an important role in oocyte transcription regulation, epigenetic modifications, and embryo development.