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CRISPR/Cas9 cell death

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https://www.readbyqxmd.com/read/29643863/mutation-in-rice-abscisic-acid2-results-in-cell-death-enhanced-disease-resistance-altered-seed-dormancy-and-development
#1
Yongxiang Liao, Que Bai, Peizhou Xu, Tingkai Wu, Daiming Guo, Yongbin Peng, Hongyu Zhang, Xiaoshu Deng, Xiaoqiong Chen, Ming Luo, Asif Ali, Wenming Wang, Xianjun Wu
Lesion mimic mutants display spontaneous cell death, and thus are valuable for understanding the molecular mechanism of cell death and disease resistance. Although a lot of such mutants have been characterized in rice, the relationship between lesion formation and abscisic acid (ABA) synthesis pathway is not reported. In the present study, we identified a rice mutant, lesion mimic mutant 9150 ( lmm9150 ), exhibiting spontaneous cell death, pre-harvest sprouting, enhanced growth, and resistance to rice bacterial and blast diseases...
2018: Frontiers in Plant Science
https://www.readbyqxmd.com/read/29621632/crispr-cas9-mediated-deletion-of-ecmih-shortens-metamorphosis-time-from-mysis-larva-to-postlarva-of-exopalaemon-carinicauda
#2
Jiquan Zhang, Fengge Song, Yuying Sun, Kuijie Yu, Jianhai Xiang
The recently emerged CRISPR/Cas9 technology is the most flexible means to produce targeted mutations at the genomic loci in a variety of organisms. In Crustaceans, molt-inhibiting hormone (MIH) is an important negative-regulatory factor and plays a key role in suppressing the molting process. However, whether precise disruption of MIH in crustacean can be achieved and successfully used to improve the development and growth has not been proved. In this research, the complementary DNA (cDNA) and genomic DNA, including flanking regions of the MIH gene (EcMIH) of ridgetail white prawn Exopalaemon carinicauda, were cloned and sequenced...
April 2, 2018: Fish & Shellfish Immunology
https://www.readbyqxmd.com/read/29621180/applications-of-crispr-cas-system-to-bacterial-metabolic-engineering
#3
REVIEW
Suhyung Cho, Jongoh Shin, Byung-Kwan Cho
The clustered regularly interspaced short palindromic repeats/CRISPR-associated (CRISPR/Cas) adaptive immune system has been extensively used for gene editing, including gene deletion, insertion, and replacement in bacterial and eukaryotic cells owing to its simple, rapid, and efficient activities in unprecedented resolution. Furthermore, the CRISPR interference (CRISPRi) system including deactivated Cas9 (dCas9) with inactivated endonuclease activity has been further investigated for regulation of the target gene transiently or constitutively, avoiding cell death by disruption of genome...
April 5, 2018: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/29615718/genetic-abrogation-of-immune-checkpoints-in-antigen-specific-cytotoxic-t-lymphocyte-as-a-potential-alternative-to-blockade-immunotherapy
#4
Chi Zhang, Yanchun Peng, Philip Hublitz, Haokang Zhang, Tao Dong
T cell function can be compromised during chronic infections or through continuous exposure to tumor antigens by the action of immune checkpoint receptors, such as programmed cell death protein 1 (PD-1). Systemic administration of blocking antibodies against the PD-1 pathway can restore T cell function, and has been approved for the treatment of several malignancies, although there is a risk of adverse immune-related side-effects. We have developed a method for generating gene knockouts in human antigen (Ag)-specific cytotoxic T-Lymphocyte (CTLs) using clustered regularly interspaced short palindromic repeats (CRISPR)/CRISPR-associated protein 9 (Cas9) genome editing...
April 3, 2018: Scientific Reports
https://www.readbyqxmd.com/read/29604290/intestinal-failure-and-aberrant-lipid-metabolism-in-patients-with-dgat1-deficiency
#5
Jorik M van Rijn, Rico Chandra Ardy, Zarife Kuloğlu, Bettina Härter, Désirée Y van Haaften-Visser, Hubert P J van der Doef, Marliek van Hoesel, Aydan Kansu, Anke H M van Vugt, Marini Ng, Freddy T M Kokke, Ana Krolo, Meryem Keçeli Başaran, Neslihan Gurcan Kaya, Aysel Ünlüsoy Aksu, Buket Dalgıç, Figen Ozcay, Zeren Baris, Renate Kain, Edwin C A Stigter, Klaske D Lichtenbelt, Maarten P G Massink, Karen J Duran, Joke B G M Verheij, Dorien Lugtenberg, Peter G J Nikkels, Henricus G F Brouwer, Henkjan J Verkade, Rene Scheenstra, Bart Spee, Edward E S Nieuwenhuis, Paul J Coffer, Andreas R Janecke, Gijs van Haaften, Roderick H J Houwen, Thomas Müller, Sabine Middendorp, Kaan Boztug
BACKGROUND & AIMS: Congenital diarrheal disorders are rare inherited intestinal disorders characterized by intractable, sometimes life-threatening, diarrhea and nutrient malabsorption; some have been associated with mutations in diacylglycerol-acyltransferase 1 (DGAT1), which catalyzes formation of triacylglycerol from diacylglycerol and acyl-CoA. We investigated the mechanisms by which DGAT1 deficiency contributes to intestinal failure using patient-derived organoids. METHODS: We collected blood samples from 10 patients, from 6 unrelated pedigrees, who presented with early-onset severe diarrhea and/or vomiting, hypoalbuminemia, and/or (fatal) protein-losing enteropathy with intestinal failure; we performed next-generation sequence analysis of DNA from 8 patients...
March 28, 2018: Gastroenterology
https://www.readbyqxmd.com/read/29601977/surf1-knockout-cloned-pigs-early-onset-of-a-severe-lethal-phenotype
#6
C Quadalti, D Brunetti, I Lagutina, R Duchi, A Perota, G Lazzari, R Cerutti, I Di Meo, M Johnson, E Bottani, P Crociara, C Corona, S Grifoni, V Tiranti, E Fernandez-Vizarra, A J Robinson, C Viscomi, C Casalone, M Zeviani, C Galli
Leigh syndrome (LS) associated with cytochrome c oxidase (COX) deficiency is an early onset, fatal mitochondrial encephalopathy, leading to multiple neurological failure and eventually death, usually in the first decade of life. Mutations in SURF1, a nuclear gene encoding a mitochondrial protein involved in COX assembly, are among the most common causes of LS. LSSURF1 patients display severe, isolated COX deficiency in all tissues, including cultured fibroblasts and skeletal muscle. Recombinant, constitutive SURF1-/- mice show diffuse COX deficiency, but fail to recapitulate the severity of the human clinical phenotype...
March 27, 2018: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/29580211/new-insight-into-the-mechanism-underlying-the-silk-gland-biological-process-by-knocking-out-fibroin-heavy-chain-in-the-silkworm
#7
Yong Cui, Yanan Zhu, Yongjian Lin, Lei Chen, Qili Feng, Wen Wang, Hui Xiang
BACKGROUND: Exploring whether and how mutation of silk protein contributes to subsequent re-allocation of nitrogen, and impacts on the timing of silk gland degradation, is important to understand silk gland biology. Rapid development and wide application of genome editing approach in the silkworm provide us an opportunity to address these issues. RESULTS: Using CRISPR/Cas9 system, we successfully performed genome editing of Bmfib-H. The loss-of-function mutations caused naked pupa and thin cocoon mutant phenotypes...
March 26, 2018: BMC Genomics
https://www.readbyqxmd.com/read/29560097/sc79-protects-dopaminergic-neurons-from-oxidative-stress
#8
Yan Xu, Ya-Wen Gao, Yu Yang
Oxidative stress could lead to dopaminergic neuronal cell death. SC79 is a novel, selective and highly-efficient Akt activator. The current study tested its effect in dopaminergic neurons with oxidative stress. In both SH-SY5Y cells and primary murine dopaminergic neurons, pre-treatment with SC79 largely inhibited hydrogen peroxide (H2 O2 )-induced cell viability reduction, apoptosis and necrosis. SC79 activated Akt in the neuronal cells, which was required for its neuroprotection against H2 O2 . Inhibition of Akt activation (by MK-2206 or AT7867) or expression (by targeted short hairpin RNA) largely attenuated SC79-induced neuroprotection...
February 27, 2018: Oncotarget
https://www.readbyqxmd.com/read/29532865/crispr-cas9-mediated-asxl1-mutations-in-u937-cells-disrupt-myeloid-differentiation
#9
Zhi-Jie Wu, Xin Zhao, Lauren G Banaszak, Fernanda Gutierrez-Rodrigues, Keyvan Keyvanfar, Shou-Guo Gao, Diego Quinones Raffo, Sachiko Kajigaya, Neal S Young
Additional sex combs-like 1 (ASXL1) is a well‑known tumor suppressor gene and epigenetic modifier. ASXL1 mutations are frequent in myeloid malignances; these mutations are risk factors for the development of myelodysplasia and also appear as small clones during normal aging. ASXL1 appears to act as an epigenetic regulator of cell survival and myeloid differentiation; however, the molecular mechanisms underlying the malignant transformation of cells with ASXL1 mutations are not well defined. Using Clustered Regularly Interspaced Short Palindromic Repeats (CRISPR)/CRISPR-associated protein-9 nuclease (Cas9) genome editing, heterozygous and homozygous ASXL1 mutations were introduced into human U937 leukemic cells...
April 2018: International Journal of Oncology
https://www.readbyqxmd.com/read/29518119/arylamine-n-acetyltransferase-1-protects-against-reactive-oxygen-species-during-glucose-starvation-role-in-the-regulation-of-p53-stability
#10
LiLi Wang, Rodney F Minchin, Neville J Butcher
Human arylamine N-acetyltransferase 1 (NAT1) has been associated with cancer cell growth and invasion, but the underlying molecular mechanisms remain unknown. NAT1 is located on the short arm of chromosome 8 (8p21), a region that is commonly deleted in colon cancer. Previously, it was reported that HT-29 colon cancer cells, which have a large deletion at 8p21-22, show marked morphological changes, increased E-cadherin expression and altered cell-cell contact inhibition following down-regulation of NAT1 with shRNA...
2018: PloS One
https://www.readbyqxmd.com/read/29491424/asc-and-caspase-8-dependent-apoptotic-pathway-diverges-from-the-nlrc4-inflammasome-in-macrophages
#11
Bettina L Lee, Kathleen M Mirrashidi, Irma B Stowe, Sarah K Kummerfeld, Colin Watanabe, Benjamin Haley, Trinna L Cuellar, Michael Reichelt, Nobuhiko Kayagaki
The NLRC4 inflammasome recognizes bacterial flagellin and components of the type III secretion apparatus. NLRC4 stimulation leads to caspase-1 activation followed by a rapid lytic cell death known as pyroptosis. NLRC4 is linked to pathogen-free auto-inflammatory diseases, suggesting a role for NLRC4 in sterile inflammation. Here, we show that NLRC4 activates an alternative cell death program morphologically similar to apoptosis in caspase-1-deficient BMDMs. By performing an unbiased genome-wide CRISPR/Cas9 screen with subsequent validation studies in gene-targeted mice, we highlight a critical role for caspase-8 and ASC adaptor in an alternative apoptotic pathway downstream of NLRC4...
February 28, 2018: Scientific Reports
https://www.readbyqxmd.com/read/29472270/crispr-rnas-trigger-innate-immune-responses-in-human-cells
#12
Sojung Kim, Taeyoung Koo, Hyeon-Gun Jee, Hee-Yeon Cho, Gyeorae Lee, Dong-Gyun Lim, Hyoung Shik Shin, Jin-Soo Kim
Here, we report that CRISPR guide RNAs (gRNAs) with a 5'-triphosphate group (5'-ppp gRNAs) produced via in vitro transcription trigger RNA-sensing innate immune responses in human and murine cells, leading to cytotoxicity. 5'-ppp gRNAs in the cytosol are recognized by DDX58, which in turn activates type I interferon responses, causing up to ∼80% cell death. We show that the triphosphate group can be removed by a phosphatase in vitro and that the resulting 5'-hydroxyl gRNAs in complex with Cas9 or Cpf1 avoid innate immune responses and can achieve targeted mutagenesis at a frequency of 95% in primary human CD4+ T cells...
February 22, 2018: Genome Research
https://www.readbyqxmd.com/read/29463237/inhibition-of-autophagy-sensitizes-cancer-cells-to-photofrin-based-photodynamic-therapy
#13
Antoni Domagala, Joanna Stachura, Magdalena Gabrysiak, Angelika Muchowicz, Radoslaw Zagozdzon, Jakub Golab, Malgorzata Firczuk
BACKGROUND: Accumulating evidence suggest that autophagy plays a pivotal role in various anticancer therapies, including photodynamic therapy (PDT), acting as a pro-death or pro-survival mechanism in a context-dependent manner. Therefore, we aimed to determine the role of autophagy in Photofrin-based PDT. METHODS: In vitro cytotoxic/cytostatic effects of PDT were evaluated with crystal violet cell viability assay. Autophagy induction was analyzed by immunoblotting and immunofluorescence using anti-LC3 antibody...
February 20, 2018: BMC Cancer
https://www.readbyqxmd.com/read/29450543/mutation-in-the-zebrafish-cct2-gene-leads-to-abnormalities-of-cell-cycle-and-cell-death-in-the-retina-a-model-of-cct2-related-leber-congenital-amaurosis
#14
Yuriko Minegishi, Naoki Nakaya, Stanislav I Tomarev
Purpose: The compound heterozygous mutations in the β subunit of chaperonin containing TCP-1 (CCT), encoded by CCT2, lead to the Leber congenital amaurosis (LCA). In this study, a cct2 mutant line of zebrafish was established to investigate the role of CCT2 mutations in LCA in vertebrates. Methods: A cct2 mutant zebrafish line was produced using the CRISPR-Cas9 system. Changes in the eyes of developing wild-type and mutant larvae were monitored using microscopy, immunostaining, TUNEL, and EdU assays...
February 1, 2018: Investigative Ophthalmology & Visual Science
https://www.readbyqxmd.com/read/29449584/crispr-whole-genome-screening-identifies-new-necroptosis-regulators-and-ripk1-alternative-splicing
#15
Marinella G Callow, Colin Watanabe, Katherine E Wickliffe, Russell Bainer, Sarah Kummerfield, Julie Weng, Trinna Cuellar, Vasantharajan Janakiraman, Honglin Chen, Ben Chih, Yuxin Liang, Benjamin Haley, Kim Newton, Michael R Costa
The necroptotic cell death pathway is a key component of human pathogen defense that can become aberrantly derepressed during tissue homeostasis to contribute to multiple types of tissue damage and disease. While formation of the necrosome kinase signaling complex containing RIPK1, RIPK3, and MLKL has been extensively characterized, additional mechanisms of its regulation and effector functions likely remain to be discovered. We screened 19,883 mouse protein-coding genes by CRISPR/Cas9-mediated gene knockout for resistance to cytokine-induced necroptosis and identified 112 regulators and mediators of necroptosis, including 59 new candidate pathway components with minimal or no effect on cell growth in the absence of necroptosis induction...
February 15, 2018: Cell Death & Disease
https://www.readbyqxmd.com/read/29446085/dr4-mediates-the-progression-invasion-metastasis-and-survival-of-colorectal-cancer-through-the-sp1-nf1-switch-axis-on-genomic-locus
#16
Shenshen Wu, Qingtao Meng, Chengcheng Zhang, Hao Sun, Runze Lu, Na Gao, Hongbao Yang, Xiaobo Li, Michael Aschner, Rui Chen
The single nucleotide polymorphism (SNP), -397G>T (rs13278062) polymorphism, in the promoter of Death Receptor 4 (DR4) had been reported to be associated with a significantly increased risk for bladder cancer. However, the association of this SNP with the risk of colorectal cancer has not been reported. In this study, we performed a case-control study in 1,078 colorectal cancer patients and 1,175 matched healthy controls to evaluate the association of the potential functional genetic variants in DR4 with risk and survival of colorectal cancer...
February 15, 2018: International Journal of Cancer. Journal International du Cancer
https://www.readbyqxmd.com/read/29445193/uncoupling-foxo3a-mitochondrial-and-nuclear-functions-in-cancer-cells-undergoing-metabolic-stress-and-chemotherapy
#17
Valentina Celestini, Tugsan Tezil, Luciana Russo, Candida Fasano, Paola Sanese, Giovanna Forte, Alessia Peserico, Martina Lepore Signorile, Giovanna Longo, Domenico De Rasmo, Anna Signorile, Raffaella Maria Gadaleta, Natasha Scialpi, Mineko Terao, Enrico Garattini, Tiziana Cocco, Gaetano Villani, Antonio Moschetta, Valentina Grossi, Cristiano Simone
While aberrant cancer cell growth is frequently associated with altered biochemical metabolism, normal mitochondrial functions are usually preserved and necessary for full malignant transformation. The transcription factor FoxO3A is a key determinant of cancer cell homeostasis, playing a dual role in survival/death response to metabolic stress and cancer therapeutics. We recently described a novel mitochondrial arm of the AMPK-FoxO3A axis in normal cells upon nutrient shortage. Here, we show that in metabolically stressed cancer cells, FoxO3A is recruited to the mitochondria through activation of MEK/ERK and AMPK, which phosphorylate serine 12 and 30, respectively, on FoxO3A N-terminal domain...
February 14, 2018: Cell Death & Disease
https://www.readbyqxmd.com/read/29435173/crispr-knock-out-of-programmed-cell-death-protein-1-enhances-anti-tumor-activity-of-cytotoxic-t-lymphocytes
#18
Zhilong Zhao, Long Shi, Wei Zhang, Jinsheng Han, Shaohui Zhang, Zexian Fu, Jianhui Cai
Programmed cell death protein 1 (PD-1) is an immune checkpoint receptor that functions to attenuate T cell activation. In this study, we knocked out (KO) PD-1 in cytotoxic T lymphocytes (CTLs) using CRISPR-Cas9 system to evaluate its effect on the anti-tumor activity of the CTLs against multiple myeloma (MM). Results show that PD-1 KO CTLs facilitate apoptosis and caspase activation of the co-cultured MM cells and enhanced MM cell death by 36% compared with the control. PD-1 KO also increased TNF-α and IFN-γ secretion of the CTLs by 2...
January 12, 2018: Oncotarget
https://www.readbyqxmd.com/read/29378335/mitochondrial-rescue-prevents-glutathione-peroxidase-dependent-ferroptosis
#19
Anja Jelinek, Lukas Heyder, Michael Daude, Matthias Plessner, Sylvia Krippner, Robert Grosse, Wibke E Diederich, Carsten Culmsee
Research into oxidative cell death is producing exciting new mechanisms, such as ferroptosis, in the neuropathologies of cerebral ischemia and hemorrhagic brain insults. Ferroptosis is an oxidative form of regulated necrotic cell death featuring glutathione (GSH) depletion, disrupted glutathione peroxidase-4 (GPX4) redox defense and detrimental lipid reactive oxygen species (ROS) formation. Further, our recent findings identified mitochondrial damage in models of oxidative glutamate toxicity, glutathione peroxidase depletion, and ferroptosis...
January 26, 2018: Free Radical Biology & Medicine
https://www.readbyqxmd.com/read/29358305/cerebral-organoids-derived-from-sandhoff-disease-induced-pluripotent-stem-cells-exhibit-impaired-neurodifferentiation
#20
Maria L Allende, Emily K Cook, Bridget C Larman, Adrienne Nugent, Jacqueline M Brady, Diane Golebiowski, Miguel Sena-Esteves, Cynthia J Tifft, Richard L Proia
Sandhoff disease, one of the GM2 gangliosidoses, is a lysosomal storage disorder characterized by the absence of beta-hexosaminidase A and B activity and the concomitant lysosomal accumulation of its substrate, GM2 ganglioside. It features catastrophic neurodegeneration and death in early childhood. How the lysosomal accumulation of ganglioside might affect the early development of the nervous system is not understood. Recently, cerebral organoids derived from induced pluripotent stem (iPS) cells have illuminated early developmental events altered by disease processes...
January 22, 2018: Journal of Lipid Research
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