Journal of Genetics and Genomics

Small peptides, big roles ‒ RALFs regulate pollen tube growth and burst in plant reproduction

Li-Yu Chen

2018, 45(3): 121-123. doi: 10.1016/j.jgg.2018.02.006

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The desumoylating enzyme sentrin-specific protease 3 contributes to myocardial ischemia reperfusion injury

Lingchen Gao, Yichao Zhao, Jie He, Yang Yan, Longwei Xu, Nan Lin, Qingqi Ji, Renyang Tong, Yanan Fu, Yu Gao, Yuanyuan Su, Ancai Yuan, Ben He, Jun Pu

2018, 45(3): 125-135. doi: 10.1016/j.jgg.2017.12.002

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Abstract:
Sentrin-specific protease 3 (SENP3), a member of the desumoylating enzyme family, is known as a redox sensor and could regulate multiple cellular signaling pathways. However, its implication in myocardial ischemia reperfusion (MIR) injury is unclear. Here, we observed that SENP3 was expressed and upregulated in the mouse heart depending on reactive oxygen species (ROS) production in response to MIR injury. By utilizing siRNA-mediated cardiac specific gene silencing, SENP3 knockdown was demonstrated to significantly reduce MIR-induced infarct size and improve cardiac function. Mechanistic studies indicated that SENP3 silencing ameliorated myocardial apoptosis mainly via suppression of endoplasmic reticulum (ER) stress and mitochondrial-mediated apoptosis pathways. By contrast, adenovirus-mediated cardiac SENP3 overexpression significantly exaggerated MIR injury. Further molecular analysis revealed that SENP3 promoted mitochondrial translocation of dynamin-related protein 1 (Drp1) in reperfused myocardium. In addition, mitochondrial division inhibitor-1 (Mdivi-1), a pharmacological inhibitor of Drp1, significantly attenuated the exaggerated mitochondrial abnormality and cardiac injury by SENP3 overexpression after MIR injury. Taken together, we provide the first direct evidence that SENP3 upregulation pivotally contributes to MIR injury in a Drp1-dependent manner, and suggest that SENP3 suppression may hold therapeutic promise for constraining MIR injury.

A novel lncRNA, Lnc-OC1, promotes ovarian cancer cell proliferation and migration by sponging miR-34a and miR-34c

Fangfang Tao, Xinxin Tian, Mengxi Lu, Zhiqian Zhang

2018, 45(3): 137-145. doi: 10.1016/j.jgg.2018.03.001

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Abstract:
Long non-coding RNAs (lncRNAs) have been reported to be of great importance in tumorigenesis and progression of a variety of cancers. However, the role of lncRNAs in ovarian cancer (OC) remains largely unknown. In the present study, we identified a novel lncRNA, LOC100288181 (named as Lnc-OC1), which acted as a key regulator in the development and progression of OC. The combined Gene Expression Omnibus (GEO) database analysis revealed that Lnc-OC1 was significantly upregulated in OC tissues and Kaplan-Meier survival analysis confirmed that high Lnc-OC1 expression was associated with poor prognosis of OC patients. Importantly, we also demonstrated that knockdown of Lnc-OC1 suppressed cell proliferation, colony formation, invasion and migrationin vitro and inhibited tumorigenicity in vivo. Mechanistically, Lnc-OC1 repressed the expression of endogenous miR-34a and miR-34c as a sponge and vice versa. Moreover, rescue experiments demonstrated that the oncogenic function of Lnc-OC1 at least partially depended on suppressing miR-34a and miR-34c. In conclusion, our results suggest that the Lnc-OC1-miR-34a/34c axis may play a pivotal role in OC, and may serve as a potential diagnostic biomarker and a powerful therapeutic target for OC.

Overexpressing dominant-negative FGFR2-IIIb impedes lung branching morphogenesis in pigs

Qin Chen, Bin Fang, Ying Wang, Chu Li, Xiaoxue Li, Ronggen Wang, Qiang Xiong, Lining Zhang, Yong Jin, Manling Zhang, Xiaorui Liu, Lin Li, Lisha Mou, Rongfeng Li, Haiyuan Yang, Yifan Dai

2018, 45(3): 147-154. doi: 10.1016/j.jgg.2018.02.002

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Genetic studies with mouse models have shown that fibroblast growth factor receptor 2-IIIb (FGFR2-IIIb) plays crucial roles in lung development and differentiation. To evaluate the effect of FGFR2-IIIb in pig lung development, we employed somatic cell nuclear transfer (SCNT) technology to generate transgenic pig fetuses overexpressing the transmembrane (dnFGFR2-IIIb-Tm) and soluble (dnFGFR2-IIIb-HFc) forms of the dominant-negative human FGFR2-IIIb driven by the human surfactant protein C (SP-C) promoter, which was specifically expressed in lung epithelia. Eight dnFGFR2-IIIb-Tm transgenic and twelve dnFGFR2-IIIb-HFc transgenic pig fetuses were collected from three and two recipient sows, respectively. Repression of FGFR2-IIIb in lung epithelia resulted in smaller lobes and retardation of alveolarization in both forms of dnFGFR2-IIIb transgenic fetuses. Moreover, the dnFGFR2-IIIb-HFc transgenic ones showed more deterioration in lung development. Our results demonstrate that disruption of FGFR2-IIIb signaling in the epithelium impedes normal branching and alveolarization in pig lungs, which is less severe than the results observed in transgenic mice. The dnFGFR2-IIIb transgenic pig is a good model for the studies of blastocyst complementation as well as the mechanisms of lung development and organogenesis.

Novel DYW-type pentatricopeptide repeat (PPR) protein BLX controls mitochondrial RNA editing and splicing essential for early seed development of Arabidopsis

Yan Sun, Jiaying Huang, Sheng Zhong, Hongya Gu, Shan He, Li-Jia Qu

2018, 45(3): 155-168. doi: 10.1016/j.jgg.2018.01.006

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In plants, RNA editing is a post-transcriptional process that changes specific cytidine to uridine in both mitochondria and plastids. Most pentatricopeptide repeat (PPR) proteins are involved in organelle RNA editing by recognizing specific RNA sequences. We here report the functional characterization of a PPR protein from the DYW subclass, Baili Xi (BLX), which contains five PPR motifs and a DYW domain. BLX is essential for early seed development, as plants lacking the BLX gene was embryo lethal and the endosperm failed to initiate cellularization. BLX was highly expressed in the embryo and endosperm, and the BLX protein was specifically localized in mitochondria, which is essential for BLX function. We found that BLX was required for the efficient editing of 36 editing sites in mitochondria. Moreover, BLX was involved in the splicing regulation of the fourth intron of nad1 and the first intron of nad2. The loss of BLX function impaired the mitochondrial function and increased the reactive oxygen species (ROS) level. Genetic complementation with truncated variants of BLX revealed that, in addition to the DYW domain, only the fifth PPR motif was essential for BLX function. The upstream sequences of the BLX-targeted editing sites are not conserved, suggesting that BLX serves as a novel and major mitochondrial editing factor (MEF) via a new non-RNA-interacting manner. This finding provides new insights into how a DYW-type PPR protein with fewer PPR motifs regulates RNA editing in plants.

Transgenerational analysis of H3K4me3 and H3K27me3 by ChIP-Seq links epigenetic inheritance to metabolism

Ke An, Fengxia Du, Hao Meng, Guochao Li, Minjie Zhang, Zongzhi Liu, Zitong Zhao, Zilong Zhang, Di Yu, Dong Wang, Caiyun Yang, Wencui Ma, Lin Yuan, Meiting Zhou, Lili Duan, Li Jin, Hui Li, Yan Zhang, Jianzhong Su, Jie Qiao, Yingli Sun

2018, 45(3): 169-172. doi: 10.1016/j.jgg.2017.11.004

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Hepatocytes in a normal adult liver are derived solely from the embryonic hepatocytes

Ce Gao, Zhihui Zhu, Yuqi Gao, Li Jan Lo, Jun Chen, Lingfei Luo, Jinrong Peng

2018, 45(3): 173-175. doi: 10.1016/j.jgg.2017.12.003

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CDK5-mediated phosphorylation of CP190 may regulate locomotor activity in adult female Drosophila

Chin-Tong Ong, Wei-Qi Lin

2018, 45(3): 177-181. doi: 10.1016/j.jgg.2017.09.012

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2018 Vol. 45, No. 3