The Solonker suture records the termination of the central Asian Orogenic Belt (CAOB). However, tectonic development of the Solonker suture is poorly understood. We report new field data for the Ondor Sum melange in the Ulan valley, and present a new evaluation of the orogenic belt extending from the southern Mongolia cratonic boundary to the north China craton within the context of a new geological framework and tectonic model, which incorporates relevant data from the literature. The southern accretionary zone between the north China craton and the Solonker suture is characterized by the Mid‐Ordovician‐Early Silurian Ulan island arc‐Ondor Sum subduction‐accretion complex and the Bainaimiao arc. This zone was consolidated by the Carboniferous‐Permian when it evolved into an Andean‐type magmatic margin above a south dipping subduction zone. The northern accretionary zone north of the Solonker suture extends southward from a Devonian to Carboniferous active continental margin, through the Hegenshan ophiolite‐arc accretionary complex to the Late Carboniferous Baolidao arc associated with some accreted Precambrian blocks. This northern zone had consolidated by the Permian when it developed into an Andean‐type magmatic margin above a north dipping subduction zone. Final subduction of the central Asian ocean caused the two opposing active continental margins to collide, leading to formation of the Solonker suture in the end‐Permian. Predominant northward subduction during final formation of the suture gave rise in the upper northern plate to a large‐scale, postcollisional, south directed thrust and fold belt in the Triassic‐Jurassic. In summary, the CAOB underwent three final stages of tectonic development: early Japanese‐type accretion, Andean‐type magmatism, and Himalayan‐type collision.

Since the initial description of induced pluripotent stem (iPS) cells created by forced expression of four transcription factors in mouse fibroblasts, the technique has been used to generate embryonic stem (ES)-cell-like pluripotent cells from a variety of cell types in other species, including primates and rat. It has become a popular means to reprogram somatic genomes into an embryonic-like pluripotent state, and a preferred alternative to somatic-cell nuclear transfer and somatic-cell fusion with ES cells. However, iPS cell reprogramming remains slow and inefficient. Notably, no live animals have been produced by the most stringent tetraploid complementation assay, indicative of a failure to create fully pluripotent cells. Here we report the generation of several iPS cell lines that are capable of generating viable, fertile live-born progeny by tetraploid complementation. These iPS cells maintain a pluripotent potential that is very close to ES cells generated from in vivo or nuclear transfer embryos. We demonstrate the practicality of using iPS cells as useful tools for the characterization of cellular reprogramming and developmental potency, and confirm that iPS cells can attain true pluripotency that is similar to that of ES cells.

N(6)-methyladenosine (m(6)A) has been recently identified as a conserved epitranscriptomic modification of eukaryotic mRNAs, but its features, regulatory mechanisms, and functions in cell reprogramming are largely unknown. Here, we report m(6)A modification profiles in the mRNA transcriptomes of four cell types with different degrees of pluripotency. Comparative analysis reveals several features of m(6)A, especially gene- and cell-type-specific m(6)A mRNA modifications. We also show that microRNAs (miRNAs) regulate m(6)A modification via a sequence pairing mechanism. Manipulation of miRNA expression or sequences alters m(6)A modification levels through modulating the binding of METTL3 methyltransferase to mRNAs containing miRNA targeting sites. Increased m(6)A abundance promotes the reprogramming of mouse embryonic fibroblasts (MEFs) to pluripotent stem cells; conversely, reduced m(6)A levels impede reprogramming. Our results therefore uncover a role for miRNAs in regulating m(6)A formation of mRNAs and provide a foundation for future functional studies of m(6)A modification in cell reprogramming.