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6. FANCM suppresses DNA replication stress at ALT telomeres by disrupting TERRA R-loops.

Author

Pan, Xiaolei, Chen, Yun, Biju, Beena, Ahmed, Naveed, Kong, Joyce, Goldenberg, Marti, Huang, Judy, Mohan, Nandakumar, Klosek, Stephanie, Parsa, Kian, Guh, Chia-Yu, Lu, Robert, Pickett, Hilda, Chu, Hsueh-Ping, and Zhang, Dong

Subjects
BRCA2 Protein, Biomarkers, Tumor, Cell Line, Tumor, DNA Damage, DNA Helicases, DNA Polymerase III, DNA Repair, DNA Replication, DNA, Single-Stranded, Fanconi Anemia Complementation Group D2 Protein, Fanconi Anemia Complementation Group N Protein, Gene Expression Regulation, Neoplastic, HeLa Cells, Humans, In Situ Hybridization, Fluorescence, Phenotype, R-Loop Structures, Rad51 Recombinase, Telomere, Telomere Homeostasis
Abstract

Cancer cells maintain their telomeres by either re-activating telomerase or adopting the homologous recombination (HR)-based Alternative Lengthening of Telomere (ALT) pathway. Among the many prominent features of ALT cells, C-circles (CC) formation is considered to be the most specific and quantifiable biomarker of ALT. However, the molecular mechanism behind the initiation and maintenance of CC formation in ALT cells is still largely unknown. We reported previously that depletion of the FANCM complex (FANCM-FAAP24-MHF1&2) in ALT cells induced pronounced replication stress, which primarily takes place at their telomeres. Here, we characterized the changes in ALT associated phenotypes in cells deficient of the FANCM complex. We found that depletion of FAAP24 or FANCM, but not MHF1&2, induces a dramatic increase of CC formation. Most importantly, we identified multiple DNA damage response (DDR) and DNA repair pathways that stimulate the dramatic increase of CC formation in FANCM deficient cells, including the dissolvase complex (BLM-TOP3A-RMI1/2, or BTR), DNA damage checkpoint kinases (ATR and Chk1), HR proteins (BRCA2, PALB2, and Rad51), as well as proteins involved in Break-Induced Replication (BIR) (POLD1 and POLD3). In addition, FANCD2, another Fanconi Anemia (FA) protein, is also required for CC formation, likely through promoting the recruitment of BLM to the replication stressed ALT telomeres. Finally, we demonstrated that TERRA R-loops accumulate at telomeres in FANCM deficient ALT cells and downregulation of which attenuates the ALT-associated PML bodies (APBs), replication stress and CC formation. Taken together, our data suggest that FANCM prevents replisomes from stalling/collapsing at ALT telomeres by disrupting TERRA R-loops.

Published
2019

31. Cardiac-specific microRNA-125b deficiency induces perinatal death and cardiac hypertrophy

Author

Sheng-Kai Chang, Chung-Yi Hu, Oi Kuan Choong, Desy S. Lee, Patrick C.H. Hsieh, Po-Ju Lin, Shu-Wha Lin, Martin W. Nicholson, Tien Hsu, Shu-Chian Ruan, Chen-Yun Chen, and Li-Wei Liu

Subjects
Proteomics, 0301 basic medicine, Molecular biology, Physiology, Perinatal Death, 030204 cardiovascular system & hematology, Mitochondrion, Mitochondria, Heart, Transcriptome, Mice, chemistry.chemical_compound, 0302 clinical medicine, Myocytes, Cardiac, Mice, Knockout, Multidisciplinary, Immunohistochemistry, Phenotype, Organ Specificity, Gene Targeting, Heart Function Tests, Knockout mouse, Medicine, RNA Interference, medicine.medical_specialty, Mitochondrial DNA, Science, Cardiomegaly, Biology, Article, 03 medical and health sciences, Internal medicine, Developmental biology, microRNA, medicine, Animals, Humans, Genetic Predisposition to Disease, Genetic Association Studies, Fatty acid metabolism, Gene Expression Profiling, Computational Biology, Embryonic stem cell, MicroRNAs, 030104 developmental biology, Endocrinology, Gene Expression Regulation, chemistry, Abnormal mitochondrial morphology
Abstract

MicroRNA-125b, the first microRNA to be identified, is known to promote cardiomyocyte maturation from embryonic stem cells; however, its physiological role remains unclear. To investigate the role of miR-125b in cardiovascular biology, cardiac-specific miR-125b-1 knockout mice were generated. We found that cardiac-specific miR-125b-1 knockout mice displayed half the miR-125b expression of control mice resulting in a 60% perinatal death rate. However, the surviving mice developed hearts with cardiac hypertrophy. The cardiomyocytes in both neonatal and adult mice displayed abnormal mitochondrial morphology. In the deficient neonatal hearts, there was an increase in mitochondrial DNA, but total ATP production was reduced. In addition, both the respiratory complex proteins in mitochondria and mitochondrial transcription machinery were impaired. Mechanistically, using transcriptome and proteome analysis, we found that many proteins involved in fatty acid metabolism were significantly downregulated in miR-125b knockout mice which resulted in reduced fatty acid metabolism. Importantly, many of these proteins are expressed in the mitochondria. We conclude that miR-125b deficiency causes a high mortality rate in neonates and cardiac hypertrophy in adult mice. The dysregulation of fatty acid metabolism may be responsible for the cardiac defect in the miR-125b deficient mice.

Published
2021

36. Use of antimicrobial peptides as a feed additive for juvenile goats

Author

Liu, Qi, primary, Yao, Shuhua, additional, Chen, Yun, additional, Gao, Shuang, additional, Yang, Yanyi, additional, Deng, Junliang, additional, Ren, Zhihua, additional, Shen, Liuhong, additional, Cui, Hengmin, additional, Hu, Yanchun, additional, Ma, Xiaoping, additional, and Yu, Shumin, additional

Published
2017
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37. DrwH, a novel WHy domain-containing hydrophobic LEA5C protein from Deinococcus radiodurans, protects enzymatic activity under oxidative stress

Author

Jiang, Shijie, primary, Wang, Jin, additional, Liu, Xiaoli, additional, Liu, Yingying, additional, Guo, Cui, additional, Zhang, Liwen, additional, Han, Jiahui, additional, Wu, Xiaoli, additional, Xue, Dong, additional, Gomaa, Ahmed E., additional, Feng, Shuai, additional, Zhang, Heng, additional, Chen, Yun, additional, Ping, Shuzhen, additional, Chen, Ming, additional, Zhang, Wei, additional, Li, Liang, additional, Zhou, Zhengfu, additional, Zuo, Kaijing, additional, Li, Xufeng, additional, Yang, Yi, additional, and Lin, Min, additional

Published
2017
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49. eIF5A1/RhoGDIα pathway: a novel therapeutic target for treatment of spinal cord injury identified by a proteomics approach

Author

Visar Belegu, Jin Liu, Yang Xu, Fei-Fei Shang, Chen-Yun Li, Wei Wang, Ting-Hua Wang, Lei Xia, Wei Liu, Wei Zhao, and Ran Liu

Subjects
Neurite, Cell Survival, Molecular Sequence Data, Primary Cell Culture, Remission, Spontaneous, Biology, Motor Activity, Article, Cell Line, Rats, Sprague-Dawley, In vivo, Peptide Initiation Factors, medicine, Initiation factor, Animals, Humans, Amino Acid Sequence, RNA, Small Interfering, Spinal cord injury, Cytoskeleton, Spinal Cord Injuries, Cell Proliferation, Neurons, rho Guanine Nucleotide Dissociation Inhibitor alpha, Gene knockdown, Multidisciplinary, Cell growth, RNA-Binding Proteins, Recovery of Function, medicine.disease, Spinal cord, Molecular biology, Cell biology, Rats, medicine.anatomical_structure, Gene Expression Regulation, Spinal Cord, Female, Signal transduction, Signal Transduction
Abstract

Spinal cord injury (SCI) is frequently accompanied by a degree of spontaneous functional recovery. The underlying mechanisms through which such recovery is generated remain elusive. In this study, we observed a significant spontaneous motor function recovery 14 to 28 days after spinal cord transection (SCT) in rats. Using a comparative proteomics approach, caudal to the injury, we detected difference in 20 proteins. Two of these proteins, are eukaryotic translation initiation factor 5A1 (eIF5A1) that is involved in cell survival and proliferation and Rho GDP dissociation inhibitor alpha (RhoGDIα), a member of Rho GDI family that is involved in cytoskeletal reorganization. After confirming the changes in expression levels of these two proteins following SCT, we showed that in vivo eIF5A1 up-regulation and down-regulation significantly increased and decreased, respectively, motor function recovery. In vitro, eIF5A1 overexpression in primary neurons increased cell survival and elongated neurite length while eIF5A1 knockdown reversed these results. We found that RhoGDIα up-regulation and down-regulation rescues the effect of eIF5A1 down-regulation and up-regulation both in vivo and in vitro. Therefore, we have identified eIF5A1/RhoGDIα pathway as a new therapeutic target for treatment of spinal cord injured patients.

Published
2015
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