Hydrogenation of Penta-Graphene Leads to Unexpected Large Improvement in Thermal Conductivity

Penta-graphene (PG) has been identified as a novel two-dimensional (2D) material with an intrinsic bandgap, which makes it especially promising for electronics applications. In this work, we use first-principles lattice dynamics and iterative solution of the phonon Boltzmann transport equation (BTE) to determine the thermal conductivity of PG and its more stable derivative, hydrogenated penta-graphene (HPG). As a comparison, we also studied the effect of hydrogenation on graphene thermal conductivity. In contrast to hydrogenation of graphene, which leads to a dramatic decrease in thermal conductivity, HPG shows a notable increase in thermal conductivity, which is much higher than that of PG. Considering the necessity of using the same thickness when comparing thermal conductivity values of different 2D materials, hydrogenation leads to a 63% reduction in thermal conductivity for graphene, while it results in a 76% increase for PG. The high thermal conductivity of HPG makes it more thermally conductive than most other semiconducting 2D materials, such as the transition metal chalcogenides. Our detailed analyses show that the primary reason for the counterintuitive hydrogenation-induced thermal conductivity enhancement is the weaker bond anharmonicity in HPG than PG. This leads to weaker phonon scattering after hydrogenation, despite the increase in the phonon scattering phase space. The high thermal conductivity of HPG may inspire intensive research around HPG and other derivatives of PG as potential materials for future nanoelectronic devices. The fundamental physics understood from this study may open up a new strategy to engineer thermal transport properties of other 2D materials by controlling bond anharmonicity via functionalization

RNA m6A methylation participates in regulation of postnatal development of the mouse cerebellum

Abstract Background N6-methyladenosine (m6A) is an important epitranscriptomic mark with high abundance in the brain. Recently, it has been found to be involved in the regulation of memory formation and mammalian cortical neurogenesis. However, while it is now established that m6A methylation occurs in a spatially restricted manner, its functions in specific brain regions still await elucidation. Results We identify widespread and dynamic RNA m6A methylation in the developing mouse cerebellum and further uncover distinct features of continuous and temporal-specific m6A methylation across the four postnatal developmental processes. Temporal-specific m6A peaks from P7 to P60 exhibit remarkable changes in their distribution patterns along the mRNA transcripts. We also show spatiotemporal-specific expression of m6A writers METTL3, METTL14, and WTAP and erasers ALKBH5 and FTO in the mouse cerebellum. Ectopic expression of METTL3 mediated by lentivirus infection leads to disorganized structure of both Purkinje and glial cells. In addition, under hypobaric hypoxia exposure, Alkbh5-deletion causes abnormal cell proliferation and differentiation in the cerebellum through disturbing the balance of RNA m6A methylation in different cell fate determination genes. Notably, nuclear export of the hypermethylated RNAs is enhanced in the cerebellum of Alkbh5-deficient mice exposed to hypobaric hypoxia. Conclusions Together, our findings provide strong evidence that RNA m6A methylation is controlled in a precise spatiotemporal manner and participates in the regulation of postnatal development of the mouse cerebellum

Additional file 6: of RNA m6A methylation participates in regulation of postnatal development of the mouse cerebellum

Table S8 GO analysis of the genes with altered m6A levels between wild-type and Alkbh5-deficient mice exposed to hypobaric hypoxia. (XLSX 83 kb

Additional file 3: of RNA m6A methylation participates in regulation of postnatal development of the mouse cerebellum

Table S5. GO analysis of genes encoded by the CMRs at P7 and P60, and SMRs at the four developmental stages. (XLSX 128 kb

Additional file 5: of RNA m6A methylation participates in regulation of postnatal development of the mouse cerebellum

Table S7 List of the 839 RNAs with strong positive or negative correlation between their methylation levels and expression levels. (XLSX 82 kb

Additional file 2: of RNA m6A methylation participates in regulation of postnatal development of the mouse cerebellum

Table S4. GO analysis of genes containing m6A ON and OFF switches during mouse cerebellar development. (XLSX 564 kb

Additional file 1: of RNA m6A methylation participates in regulation of postnatal development of the mouse cerebellum

Figure S1. Dynamic RNA methylation in the developing mouse cerebellum. Figure S2. Comparison between continuous and temporal-specific methylation during mouse cerebellar development. Figure S3. Comparison of RNA methylation between P7 and P60 based on m6A peaks identified using MACS2. Figure S4. Correlation between RNA methylation and gene expression during cerebellar development. Figure S5. Morphology analysis of mouse cerebellum upon lentivirus infection for Mettl3 overexpression. Figure S6. Phenotype analysis of the cerebellum in the WT and KO mice under normoxic condition. Figure S7. Morphology analysis of the cerebellum in WT and KO mice exposed to hypobaric hypoxia and normoxia successively. Figure S8. Dysregulated RNA methylation resulting from Alkbh5 deficiency in mouse cerebellum exposed to hypobaric hypoxia. Table S1. Data quality and processing information of m6A-seq of poly(A) RNA from wild-type mouse cerebellum (P7, P14, P21, and P60), the cerebellum of wild-type (WT) and Alkbh5 knockout (KO) mice exposed to hypobaric hypoxia (P7). Table S2. Statistics of m6A peaks and expressed RNAs in wild-type mouse cerebellum (P7, P14, P21, and P60), the cerebellum of wild-type (WT) and Alkbh5 knockout (KO) mice exposed to hypobaric hypoxia (P7). Table S3. Numbers of m6A peaks located in different regions of mRNA transcripts in wild-type mouse cerebellum at P7, P14, P21, and P60. Table S9. List of antibodies and their applications used in this study. Table S10. List of primers for RT-qPCR used in this study. (PDF 14643 kb