The surface structure and chemistry of semiconductor single crystals are crucial to optoelectronic and nanoelectronic devices. Unfortunately, little is known about the native surfaces of perovskite single crystals grown by solution-based methods. Here, we found that a textured surface with characteristic striations and pyramidal pits is often present on the native surface of MAPbI3 single crystal (SC), both of which result from an unexpected etching process due to the unsaturated solution residing at the surface. The striations reflect the instantaneous fluctuations of the vicinal growth planes for a particular growth sector. The etch pits originate from the outcrops of the edge dislocations and are featured with a rectangle pyramidal shape at the (100), (010), and {112} faces as well as a square pyramidal shape at the (110) surface plane. Such two characteristic features, especially for the etch pits that could derive the dislocation density (around 104–105 cm–2 for MAPbI3 SC at the (100) surface), could be used as standard methods to evaluate the quality of organic–inorganic halide perovskite SCs. The native surface morphology with the presence of both striations and pits is strongly dependent on the details of the SC taken-out process from the growth solution and the quality of the as-grown SC, which could be the main reason for wide variations in different reported surface morphologies and hence electrical properties of SC devices.

Aim Low-grade glioma (LGG), which is the second most frequent adult brain malignancy, severely threatens patients’ health and has a high recurrence rate. Histone H3/H4 chaperone anti-silencing function 1 B ( ASF1B ) has a tight association with the initiation and development of tumours. The expression and regulation mechanism of ASF1B in LGG were discussed. Methods ASF1B expression in LGG patients as well as the association of ASF1B with overall survival and disease-free survival of LGG patients were predicted by GEPIA database. The independent prognostic value of ASF1B in LGG patients was investigated by TCGA database. RT-qPCR, together with western blot was applied for the assessment of ASF1B in LGG cell lines. After ASF1B expression was inhibited, CCK8 and colony formation assays judged cell proliferation. Flow cytometry analysis and TUNEL assay appraised cell cycle as well as apoptosis. Cell migratory and invasive capacities were measured by wound healing as well as Transwell assays. Western blot tested the expression of proliferation-, cycle-, apoptosis-, and metastasis-associated proteins. STRING and GeneMANIA database predicted the relationship between ASF1B and tousled-like kinase 1 ( TLK1) . ChIP assay testified the affinity of ASF1B with TLK1. Subsequently, TLK1 was overexpressed and ASF1B expression interfered, and the functional assays were executed. Results ASF1B was discovered to be increased in LGG tissues and cells and indicates an unfavourable prognosis for LGG patients. ASF1B was not an independent prognostic factor for LGG. ASF1B deficiency obstructed the proliferation, cell cycle as well as metastasis of LGG cells, and induced cell death, which might be realized through the interaction with TLK1 . Conclusion The interaction between ASF1B and TLK1 promoted the malignant progression of LGG. Key messages TLK1 interacts with ASF1B. Interference with ASF1B inhibits the proliferative, invasive and migratory capabilities and induces the cycle arrest, along with the apoptosis of LGG cells. The interaction between ASF1B and TLK1 promotes the malignant progression of LGG.