Microstructure evolution and hardening effect of pure tungsten and W-1.5%ZrO_(2) alloy under carbon ion irradiation are investigated by using transmission electron microscopy and nano-indentation.Carbon ion irradiatio...Microstructure evolution and hardening effect of pure tungsten and W-1.5%ZrO_(2) alloy under carbon ion irradiation are investigated by using transmission electron microscopy and nano-indentation.Carbon ion irradiation is performed at 700℃ with irradiation damages ranging from 0.25 dpa to 2.0 dpa.The results show that the irradiation defect clusters are mainly in the form of dislocation loop.The size and density of dislocation loops increase with irradiation damages intensifying.The W-1.5%ZrO_(2) alloy has a smaller dislocation loop size than that of pure tungsten.It is proposed that the phase boundaries have the ability to absorb and annihilate defects and the addition of ZrO_(2) phase improves the sink strength for irradiation defects.It is confirmed that the W-1.5% ZrO_(2) alloy shows a smaller change in hardness than the pure tungsten after being irradiated.From the above results,we conclude that the addition of ZrO_(2) into tungsten can significantly reduce the accumulation of irradiated defects and improve the irradiation resistance behaviors of the tungsten materials.展开更多
Stimulatory regulators for DNA methyltransferase activity,such as Dnmt3L and some Dnmt3b isoforms,affect DNA methylation patterns,thereby maintaining gene body methylation and maternal methylation imprinting,as well a...Stimulatory regulators for DNA methyltransferase activity,such as Dnmt3L and some Dnmt3b isoforms,affect DNA methylation patterns,thereby maintaining gene body methylation and maternal methylation imprinting,as well as the methylation landscape of pluripotent cells.Here we show that metastasis-related methyltransferase 1(Merm1),a protein deleted in individuals with Williams-Beuren syndrome,acts as a repressive regulator of Dnmt3a.Merm1 interacts with Dnmt3a and represses its methyltransferase activity with the requirement of the binding motif for S-adenosyl-L-methionine.Functional analysis of gene regulation revealed that Merm1 is capable of maintaining hypomethylated rRNA gene bodies and co-localizes with RNA polymerase I in the nucleolus.Dnmt3a recruits Merml,and in return,Merml ensures the binding of Dnmt3a to hypomethylated gene bodies.Such interplay between Dnmt3a and Merml facilitates transcriptional elongation by RNA polymerase I.Our findings reveal a repressive factor for Dnmt3a and uncover a molecular mechanism underlying transcriptional elongation of rRNA genes.展开更多
基金Project supported by the President's Foundation of the ChinaAcademy of Engineering Physics(Grant No.YZJJLX2018003)the National Natural Science Foundation of China(Grant Nos.U2004180 and 12105261)the Program for Changjiang Scholars and Innovative Research Team in Universities,China(Grant No.IRT1234).
文摘Microstructure evolution and hardening effect of pure tungsten and W-1.5%ZrO_(2) alloy under carbon ion irradiation are investigated by using transmission electron microscopy and nano-indentation.Carbon ion irradiation is performed at 700℃ with irradiation damages ranging from 0.25 dpa to 2.0 dpa.The results show that the irradiation defect clusters are mainly in the form of dislocation loop.The size and density of dislocation loops increase with irradiation damages intensifying.The W-1.5%ZrO_(2) alloy has a smaller dislocation loop size than that of pure tungsten.It is proposed that the phase boundaries have the ability to absorb and annihilate defects and the addition of ZrO_(2) phase improves the sink strength for irradiation defects.It is confirmed that the W-1.5% ZrO_(2) alloy shows a smaller change in hardness than the pure tungsten after being irradiated.From the above results,we conclude that the addition of ZrO_(2) into tungsten can significantly reduce the accumulation of irradiated defects and improve the irradiation resistance behaviors of the tungsten materials.
文摘Stimulatory regulators for DNA methyltransferase activity,such as Dnmt3L and some Dnmt3b isoforms,affect DNA methylation patterns,thereby maintaining gene body methylation and maternal methylation imprinting,as well as the methylation landscape of pluripotent cells.Here we show that metastasis-related methyltransferase 1(Merm1),a protein deleted in individuals with Williams-Beuren syndrome,acts as a repressive regulator of Dnmt3a.Merm1 interacts with Dnmt3a and represses its methyltransferase activity with the requirement of the binding motif for S-adenosyl-L-methionine.Functional analysis of gene regulation revealed that Merm1 is capable of maintaining hypomethylated rRNA gene bodies and co-localizes with RNA polymerase I in the nucleolus.Dnmt3a recruits Merml,and in return,Merml ensures the binding of Dnmt3a to hypomethylated gene bodies.Such interplay between Dnmt3a and Merml facilitates transcriptional elongation by RNA polymerase I.Our findings reveal a repressive factor for Dnmt3a and uncover a molecular mechanism underlying transcriptional elongation of rRNA genes.
