Current Articles

Recollection
Chia-Chen Tan and genetics in modern China
Lei Fu
2019, 10(5): 313-314. doi: 10.1007/s13238-018-0539-2
Abstract:
Review
Remodeling of host membranes during herpesvirus assembly and egress
Ying Lv, Sheng Zhou, Shengyan Gao, Hongyu Deng
2019, 10(5): 315-326. doi: 10.1007/s13238-018-0577-9
Abstract:
Many viruses, enveloped or non-enveloped, remodel host membrane structures for their replication, assembly and escape from host cells. Herpesviruses are important human pathogens and cause many diseases. As large enveloped DNA viruses, herpesviruses undergo several complex steps to complete their life cycles and produce infectious progenies. Firstly, herpesvirus assembly initiates in the nucleus, producing nucleocapsids that are too large to cross through the nuclear pores. Nascent nucleocapsids instead bud at the inner nuclear membrane to form primary enveloped virions in the perinuclear space followed by fusion of the primary envelopes with the outer nuclear membrane, to translocate the nucleocapsids into the cytoplasm. Secondly, nucleocapsids obtain a series of tegument proteins in the cytoplasm and bud into vesicles derived from host organelles to acquire viral envelopes. The vesicles are then transported to and fuse with the plasma membrane to release the mature virions to the extracellular space. Therefore, at least two budding and fusion events take place at cellular membrane structures during herpesviruses assembly and egress, which induce membrane deformations. In this review, we describe and discuss how herpesviruses exploit and remodel host membrane structures to assemble and escape from the host cell.
Research articles
Dgcr8 deletion in the primitive heart uncovered novel microRNA regulating the balance of cardiac-vascular gene program
Xi Chen, Lin Wang, Rujin Huang, Hui Qiu, Peizhe Wang, Daren Wu, Yonglin Zhu, Jia Ming, Yangming Wang, Jianbin Wang, Jie Na
2019, 10(5): 327-346. doi: 10.1007/s13238-018-0572-1
Abstract:
Primitive mammalian heart transforms from a single tube to a four-chambered muscular organ during a short developmental window. We found that knocking out global microRNA by deleting Dgcr8 microprocessor in Mesp1 cardiovascular progenitor cells lead to the formation of extremely dilated and enlarged heart due to defective cardiomyocyte (CM) differentiation. Transcriptome analysis revealed unusual upregulation of vascular gene expression in Dgcr8 cKO hearts. Single cell RNA sequencing study further confirmed the increase of angiogenesis genes in single Dgcr8 cKO CM. We also performed global microRNA profiling of E9.5 heart for the first time, and identified that miR-541 was transiently highly expressed in E9.5 hearts. Interestingly, introducing miR-541 back into microRNA-free CMs partially rescued their defects, downregulated angiogenesis genes and significantly upregulated cardiac genes. Moreover, miR-541 can target Ctgf and inhibit endothelial function. Our results suggest that microRNAs are required to suppress abnormal angiogenesis gene program to maintain CM differentiation.
Loss-of-function of sox3 causes follicle development retardation and reduces fecundity in zebrafish
Qiang Hong, Cong Li, Ruhong Ying, Heming Lin, Jingqiu Li, Yu Zhao, Hanhua Cheng, Rongjia Zhou
2019, 10(5): 347-364. doi: 10.1007/s13238-018-0603-y
Abstract:
Folliculogenesis is essential for production of female gametes in vertebrates. However, the molecular mechanisms underlying follicle development, particularly apoptosis regulation in ovary, remain elusive. Here, we generated sox3 knockout zebrafish lines using CRISPR/Cas9. sox3 knockout led to follicle development retardation and a reduced fecundity in females. Comparative analysis of transcriptome between sox3-/- and wild-type ovaries revealed that Sox3 was involved in pathways of ovarian steroidogenesis and apoptosis. Knockout of sox3 promoted follicle apoptosis and obvious apoptosis signals were detected in somatic cells of stages Ⅲ and IV follicles of sox3-/- ovaries. Moreover, Sox3 can bind to and activate the promoter of cyp19a1a. Up-regulation of Cyp19a1a expression promoted 17β-estradiol synthesis, which inhibited apoptosis in follicle development. Thus, Sox3 functions as a regulator of Cyp19a1a expression, via 17β-E2 linking apoptosis suppression, which is implicated in improving female fecundity.
Letters
Cryo-EM structure of L-fucokinase/GDP-fucose pyrophosphorylase (FKP) in Bacteroides fragilis
Ying Liu, Huifang Hu, Jia Wang, Qiang Zhou, Peng Wu, Nieng Yan, Hong-Wei Wang, Jia-Wei Wu, Linfeng Sun
2019, 10(5): 365-369. doi: 10.1007/s13238-018-0576-x
Abstract:
Single senescent cell sequencing reveals heterogeneity in senescent cells induced by telomere erosion
Huanyin Tang, Anke Geng, Tengjiao Zhang, Chen Wang, Ying Jiang, Zhiyong Mao
2019, 10(5): 370-375. doi: 10.1007/s13238-018-0591-y
Abstract:
Unc-51-like kinase (ULK) complexindependent autophagy induced by hypoxia
Yan Feng, Helen H. Kang, Pui-Mun Wong, Minghui Gao, Ping Wang, Xuejun Jiang
2019, 10(5): 376-381. doi: 10.1007/s13238-018-0584-x
Abstract:
Phosphorylation of PLIN3 by AMPK promotes dispersion of lipid droplets during starvation
Jianxi Zhu, Mingyang Xu, Yi Liu, Lisha Zhuang, Kejun Ying, Feng Liu, Dan Liu, Wenbin Ma, Zhou Songyang
2019, 10(5): 382-387. doi: 10.1007/s13238-018-0593-9
Abstract:

Current Issue

May, 2019

Volume 10, Issue 5

Pages 313-387

About the cover

Left image:a mouse E9.5 embryo with Dgcr8 microRNA microprocessor conditionally knocked out in the heart. The heart in green was extremely dilated. Top right:cTnT immunostaining (in green) showed that the heart had very thin wall. Middle right:cTnT immunostaining (in red) showed lack of sarcomere structure in a microRNA free cardiomyocyte (CM). Insert:slow calcium transient frequency. Bottom right: transfection of miR-541 rescued sarcomere structure in Dgcr8 cKO CMs. cTnT immunostaining (in red) showed typical sarcomere structure. Insert:fast calcium transient frequency.

Institute of Biophysics, Chinese Academy of Sciences, 15 Datun Road, Chaoyang Beijing 100101, China

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