scholarly journals Ctf4 organizes sister replisomes and Pol α into a replication factory

2019 ◽  
Author(s):  
Zuanning Yuan ◽  
Roxana Georgescu ◽  
Ruda de Luna Almeida Santos ◽  
Daniel Zhang ◽  
Lin Bai ◽  
...  
Keyword(s):  
Current View ◽  
Replication Factory

ABSTRACTThe current view is that eukaryotic replisomes are independent. Here we show that Ctf4 tightly dimerizes CMG helicase, with an extensive interface involving Psf2, Cdc45, and Sld5. Interestingly, Ctf4 binds only one Pol α-primase. Thus, Ctf4 may have evolved as a trimer to organize two helicases and one Pol α-primase into a replication factory. In the 2CMG-Ctf43-1Pol α-primase factory model, the two CMGs nearly face each other, placing the two lagging strands toward the center and two leading strands out the sides. The single Pol α-primase is centrally located and may prime both sister replisomes. The Ctf4-coupled-sister replisome model is consistent with cellular microscopy studies revealing two sister forks of an origin remain attached and are pushed forward from a protein platform. The replication factory model may facilitate parental nucleosome transfer during replication.

scholarly journals Ctf4 organizes sister replisomes and Pol α into a replication factory

eLife ◽  
2019 ◽  
Vol 8 ◽  
Author(s):  
Zuanning Yuan ◽  
Roxana Georgescu ◽  
Ruda de Luna Almeida Santos ◽  
Daniel Zhang ◽  
Lin Bai ◽  
...  
Keyword(s):  
Current View ◽  
Replication Factory

The current view is that eukaryotic replisomes are independent. Here we show that Ctf4 tightly dimerizes CMG helicase, with an extensive interface involving Psf2, Cdc45, and Sld5. Interestingly, Ctf4 binds only one Pol α-primase. Thus, Ctf4 may have evolved as a trimer to organize two helicases and one Pol α-primase into a replication factory. In the 2CMG–Ctf43–1Pol α-primase factory model, the two CMGs nearly face each other, placing the two lagging strands toward the center and two leading strands out the sides. The single Pol α-primase is centrally located and may prime both sister replisomes. The Ctf4-coupled-sister replisome model is consistent with cellular microscopy studies revealing two sister forks of an origin remain attached and are pushed forward from a protein platform. The replication factory model may facilitate parental nucleosome transfer during replication.

Current view on retinal OCT imaging nomenclature and terminology

2020 ◽  
Vol 87 (4) ◽  
pp. 62-68
Author(s):  
N.S. Lutsenko ◽  
◽  
O.A. Rudycheva ◽  
O.A. Isakova ◽  
T.S. Kyrylova ◽  
...  
Keyword(s):  
Current View ◽  
Oct Imaging

How the Current View of the Air and Space Environment Influences Developments of Military Space Forces.

1998 ◽  
Author(s):  
Lyndon S. Anderson ◽  
Stephen M. Rothstein
Keyword(s):  
Space Environment ◽  
Current View

CURRENT VIEW OF THE ACTION MECHANISMS AND CLINICAL USE OF XENON INHALATIONS FOR THE PURPOSES OF NEUTROPROTECTION

2020 ◽  
Vol 54 (2) ◽  
pp. 22-29
Author(s):  
L.Yu. Marchenko ◽  
◽  
E.E. Sigaleva ◽  
E.I. Matsnev ◽  
D.A. Anikeev ◽  
...  
Keyword(s):  
Current View ◽  
Clinical Use ◽  
Action Mechanisms

Aneurysmal subarachnoid hemorrhages — a current view on the diagnosis, clinical picture, treatment

2018 ◽  
Vol 0 (8.87) ◽  
pp. 98-101
Author(s):  
I.S. Zozulia ◽  
A.I. Zozulia ◽  
A.O. Volosovets ◽  
A.O. Kaminskyi
Keyword(s):  
Clinical Picture ◽  
Current View ◽  
Subarachnoid Hemorrhages ◽  
A Current

scholarly journals The Current View of Nonalcoholic Fatty Liver Disease-Related Hepatocellular Carcinoma

Cancers ◽  
2021 ◽  
Vol 13 (3) ◽  
pp. 516
Author(s):  
Tomomi Kogiso ◽  
Katsutoshi Tokushige
Keyword(s):  
Hepatocellular Carcinoma ◽  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Fatty Liver Disease ◽  
Current View ◽  
Nonalcoholic Fatty Liver ◽  
Obesity And Diabetes ◽  
Life Threatening ◽  
Lifestyle Related Diseases

Nonalcoholic fatty liver disease (NAFLD) is the hepatic manifestation of metabolic syndrome and can develop into hepatocellular carcinoma (HCC). The incidence of NAFLD-related HCC, which is accompanied by life-threatening complications, is increasing. Advanced fibrosis and lifestyle-related and metabolic comorbidities, especially obesity and diabetes mellitus, are associated with HCC development. However, HCC is also observed in the non-cirrhotic liver. Often, diagnosis is delayed until the tumor is relatively large and the disease is advanced; an effective screening or surveillance method is urgently required. Recently, the NAFLD/nonalcoholic steatohepatitis (NASH) guidelines of Japan were revised to incorporate new strategies and evidence for the management and surveillance of NAFLD/NASH. Fibrosis must be tested for noninvasively, and the risk of carcinogenesis must be stratified. The treatment of lifestyle-related diseases is expected to reduce the incidence of NAFLD and prevent liver carcinogenesis.

scholarly journals Current view and perspectives in viroid replication

2021 ◽  
Vol 47 ◽  
pp. 32-37
Author(s):  
Ying Wang
Keyword(s):  
Current View ◽  
Viroid Replication

scholarly journals Chromosomal Lesion Suppression and Removal in Escherichia coli via Linear DNA Degradation

Genetics ◽  
2003 ◽  
Vol 163 (4) ◽  
pp. 1255-1271 ◽  
Author(s):  
Anabel Miranda ◽  
Andrei Kuzminov
Keyword(s):  
Dna Degradation ◽  
Dna Helicase ◽  
Structural Element ◽  
E Coli ◽  
Linear Dna ◽  
Replication Factory ◽  
Low Copy Number ◽  
Chromosomal Lesion ◽  
Recbcd Enzyme

Abstract RecBCD is a DNA helicase/exonuclease implicated in degradation of foreign linear DNA and in RecA-dependent recombinational repair of chromosomal lesions in E. coli. The low viability of recA recBC mutants vs. recA mutants indicates the existence of RecA-independent roles for RecBCD. To distinguish among possible RecA-independent roles of the RecBCD enzyme in replication, repair, and DNA degradation, we introduced wild-type and mutant combinations of the recBCD chromosomal region on a low-copy-number plasmid into a ΔrecA ΔrecBCD mutant and determined the viability of resulting strains. Our results argue against ideas that RecBCD is a structural element in the replication factory or is involved in RecA-independent repair of chromosomal lesions. We found that RecBCD-catalyzed DNA degradation is the only activity important for the recA-independent viability, suggesting that degradation of linear tails of σ-replicating chromosomes could be one of the RecBCD’s roles. However, since the weaker DNA degradation capacity due a combination of the RecBC helicase and ssDNA-specific exonucleases restores viability of the ΔrecA ΔrecBCD mutant to a significant extent, we favor suppression of chromosomal lesions via linear DNA degradation at reversed replication forks as the major RecA-independent role of the RecBCD enzyme.

scholarly journals Cellular Signal Transductions and Their Inhibitors Derived from Deep-Sea Organisms

Marine Drugs ◽  
2021 ◽  
Vol 19 (4) ◽  
pp. 205
Author(s):  
Liyan Wang ◽  
Kazuo Umezawa
Keyword(s):  
Cell Signaling ◽  
Anticancer Agents ◽  
Deep Sea ◽  
Antimicrobial Agents ◽  
Biological Activities ◽  
Bioactive Metabolites ◽  
Current View ◽  
Cellular Signal ◽  
Signaling Inhibitors ◽  
Signal Transductions

Not only physiological phenomena but also pathological phenomena can now be explained by the change of signal transduction in the cells of specific tissues. Commonly used cellular signal transductions are limited. They consist of the protein–tyrosine kinase dependent or independent Ras-ERK pathway, and the PI3K-Akt, JAK-STAT, SMAD, and NF-κB-activation pathways. In addition, biodegradation systems, such as the ubiquitin–proteasome pathway and autophagy, are also important for physiological and pathological conditions. If we can control signaling for each by a low-molecular-weight agent, it would be possible to treat diseases in new ways. At present, such cell signaling inhibitors are mainly looked for in plants, soil microorganisms, and the chemical library. The screening of bioactive metabolites from deep-sea organisms should be valuable because of the high incidence of finding novel compounds. Although it is still an emerging field, there are many successful examples, with new cell signaling inhibitors. In this review, we would like to explain the current view of the cell signaling systems important in diseases, and show the inhibitors found from deep-sea organisms, with their structures and biological activities. These inhibitors are possible candidates for anti-inflammatory agents, modulators of metabolic syndromes, antimicrobial agents, and anticancer agents.

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