2017 Vol. 8, No. 10

News and views
The excessive response: a preparation for harder conditions
Yaguang Ren, Chao Zhang
2017, 8(10): 707-710. doi: 10.1007/s13238-017-0454-y
Li BO-Pioneer of Ecology in China
Zhicheng Gao
2017, 8(10): 711-712. doi: 10.1007/s13238-016-0286-1
Potential coordination role between O-GlcNAcylation and epigenetics
Donglu Wu, Yong Cai, Jingji Jin
2017, 8(10): 713-723. doi: 10.1007/s13238-017-0416-4
Dynamic changes of the post-translational O-GlcNAc modification (O-GlcNAcylation) are controlled by O-linked β-N-acetylglucosamine (O-GlcNAc) transferase (OGT) and the glycoside hydrolase O-GlcNAcase (OGA) in cells. O-GlcNAcylation often occurs on serine (Ser) and threonine (Thr) residues of the specific substrate proteins via the addition of O-GlcNAc group by OGT. It has been known that O-GlcNAcylation is not only involved in many fundamental cellular processes, but also plays an important role in cancer development through various mechanisms. Recently, accumulating data reveal that O-GlcNAcylation at histones or non-histone proteins can lead to the start of the subsequent biological processes, suggesting that O-GlcNAcylation as ‘protein code’ or ‘histone code’ may provide recognition platforms or executive instructions for subsequent recruitment of proteins to carry out the specific functions. In this review, we summarize the interaction of O-GlcNAcylation and epigenetic changes, introduce recent research findings that link crosstalk between OGlcNAcylation and epigenetic changes, and speculate on the potential coordination role of O-GlcNAcylation with epigenetic changes in intracellular biological processes.
Molecular barriers to direct cardiac reprogramming
Haley Vaseghi, Jiandong Liu, Li Qian
2017, 8(10): 724-734. doi: 10.1007/s13238-017-0402-x
Myocardial infarction afflicts close to three quarters of a million Americans annually, resulting in reduced heart function, arrhythmia, and frequently death. Cardiomyocyte death reduces the heart's pump capacity while the deposition of a non-conductive scar incurs the risk of arrhythmia. Direct cardiac reprogramming emerged as a novel technology to simultaneously reduce scar tissue and generate new cardiomyocytes to restore cardiac function. This technology converts endogenous cardiac fibroblasts directly into induced cardiomyocyte-like cells using a variety of cocktails including transcription factors, microRNAs, and small molecules. Although promising, direct cardiac reprogramming is still in its fledging phase, and numerous barriers have to be overcome prior to its clinical application. This review discusses current findings to optimize reprogramming efficiency, including reprogramming factor cocktails and stoichiometry, epigenetic barriers to cell fate reprogramming, incomplete conversion and residual fibroblast identity, requisite growth factors, and environmental cues. Finally, we address the current challenges and future directions for the field.
Research articles
Mammalian mitochondrial RNAs are degraded in the mitochondrial intermembrane space by RNASET2
Peipei Liu, Jinliang Huang, Qian Zheng, Leiming Xie, Xinping Lu, Jie Jin, Geng Wang
2017, 8(10): 735-749. doi: 10.1007/s13238-017-0448-9
Mammalian mitochondrial genome encodes a small set of tRNAs, rRNAs, and mRNAs. The RNA synthesis process has been well characterized. How the RNAs are degraded, however, is poorly understood. It was long assumed that the degradation happens in the matrix where transcription and translation machineries reside. Here we show that contrary to the assumption, mammalian mitochondrial RNA degradation occurs in the mitochondrial intermembrane space (IMS) and the IMSlocalized RNASET2 is the enzyme that degrades the RNAs. This provides a new paradigm for understanding mitochondrial RNA metabolism and transport.
MicroRNAs recruit eIF4E2 to repress translation of target mRNAs
Shaohong Chen, Guangxia Gao
2017, 8(10): 750-761. doi: 10.1007/s13238-017-0444-0
MicroRNAs (miRNAs) recruit the RNA-induced silencing complex (RISC) to repress the translation of target mRNAs. While the 5' 7-methylguanosine cap of target mRNAs has been well known to be important for miRNA repression, the underlying mechanism is not clear. Here we show that TNRC6A interacts with eIF4E2, a homologue of eIF4E that can bind to the cap but cannot interact with eIF4G to initiate translation, to inhibit the translation of target mRNAs. Downregulation of eIF4E2 relieved miRNA repression of reporter expression. Moreover, eIF4E2 downregulation increased the protein levels of endogenous IMP1, PTEN and PDCD4, whose expression are repressed by endogenous miRNAs. We further provide evidence showing that miRNA enhances eIF4E2 association with the target mRNA. We propose that miRNAs recruit eIF4E2 to compete with eIF4E to repress mRNA translation.
Structural and biochemical characterization of DAXX-ATRX interaction
Zhuang Li, Dan Zhao, Bin Xiang, Haitao Li
2017, 8(10): 762-766. doi: 10.1007/s13238-017-0463-x
Structural basis for DAXX interaction with ATRX
Xiaoman Wang, Yiyue Zhao, Jian Zhang, Yong Chen
2017, 8(10): 767-771. doi: 10.1007/s13238-017-0462-y
Highly efficient base editing in human tripronuclear zygotes
Changyang Zhou, Meiling Zhang, Yu Wei, Yidi Sun, Yun Sun, Hong Pan, Ning Yao, Wanxia Zhong, Yixue Li, Weiping Li, Hui Yang, Zi-jiang Chen
2017, 8(10): 772-775. doi: 10.1007/s13238-017-0459-6
Highly efficient and precise base editing in discarded human tripronuclear embryos
Guanglei Li, Yajing Liu, Yanting Zeng, Jianan Li, Lijie Wang, Guang Yang, Dunjin Chen, Xiaoyun Shang, Jia Chen, Xingxu Huang, Jianqiao Liu
2017, 8(10): 776-779. doi: 10.1007/s13238-017-0458-7
Preferential distribution of nuclear MAPK signal in α/β core neurons during long-term memory consolidation in Drosophila
Wantong Hu, Xuchen Zhang, Lianzhang Wang, Zhong-Jian Liu, Yi Zhong, Qian Li
2017, 8(10): 780-783. doi: 10.1007/s13238-017-0404-8