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2 episodes with DNA replication
2 episodes with DNA replication
2 episodes with DNA replication
2 episodes with DNA replication
2 episodes with DNA replication
11 episodes with DNA replication
4 episodes with DNA replication
3 episodes with DNA replication
In this episode, we review the high-yield topic of DNA Replication from the Biochemistry section.Follow Medbullets on social media:Facebook: www.facebook.com/medbulletsInstagram: www.instagram.com/medbulletsofficialTwitter: www.twitter.com/medbullets
Let's learn about DNA Replication and the Cell Cycle.
In this episode of the Epigenetics Podcast, we talked with Dr. Stephan Hamperl from the Helmholtz Zentrum Munich about his work on how conflicts between transcription, replication, and R-loop formation influence genome stability in human cells. During the early stages of his career Stephan studied conflicts between transcription and replication in human cells, particularly focusing on R-loop structures. In our discussion, he explains the formation of R-loops and their impact on genome stability, emphasizing the importance of the orientation of replication forks approaching R-loops in determining DNA damage outcomes. Stephan then delves into his work on the MATAC-Seq method, which analyzes chromatin domains at DNA replication origins to understand replication timing variability. The method involves methylating DNA linkers between nucleosomes and using nanopore sequencing for single-molecule readouts, revealing heterogeneity in chromatin structure at replication origins. Finally, Stephan discusses his automated image analysis pipeline for quantifying transcription and replication activity overlap in mammalian genomes, addressing the challenge of visualizing these processes simultaneously. The conversation concludes with insights into Stefan's future research directions, focusing on understanding transcription-replication conflicts' molecular basis and their potential implications in cancer cell transformation. References Hamperl, S., Brown, C. R., Garea, A. V., Perez-Fernandez, J., Bruckmann, A., Huber, K., Wittner, M., Babl, V., Stoeckl, U., Deutzmann, R., Boeger, H., Tschochner, H., Milkereit, P., & Griesenbeck, J. (2014). Compositional and structural analysis of selected chromosomal domains from Saccharomyces cerevisiae. Nucleic acids research, 42(1), e2. https://doi.org/10.1093/nar/gkt891 Hamperl, S., Bocek, M. J., Saldivar, J. C., Swigut, T., & Cimprich, K. A. (2017). Transcription-Replication Conflict Orientation Modulates R-Loop Levels and Activates Distinct DNA Damage Responses. Cell, 170(4), 774–786.e19. https://doi.org/10.1016/j.cell.2017.07.043 Chanou, A., Weiβ, M., Holler, K., Sajid, A., Straub, T., Krietsch, J., Sanchi, A., Ummethum, H., Lee, C. S. K., Kruse, E., Trauner, M., Werner, M., Lalonde, M., Lopes, M., Scialdone, A., & Hamperl, S. (2023). Single molecule MATAC-seq reveals key determinants of DNA replication origin efficiency. Nucleic acids research, 51(22), 12303–12324. https://doi.org/10.1093/nar/gkad1022 Contact Epigenetics Podcast on X Epigenetics Podcast on Instagram Epigenetics Podcast on Mastodon Epigenetics Podcast on Bluesky Epigenetics Podcast on Threads Active Motif on X Active Motif on LinkedIn Email: podcast@activemotif.com
Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.07.18.549463v1?rss=1 Authors: de Jaime Soguero, A., Hattemer, J., Haas, A., Bufe, A., Di Marco, B., Bohly, N., Landry, J. J. M., Schoell, B., Rosa, V. S., Villacorta, L., Baskan, Y., Androulaki, S., Trapp, M., Benes, V., Das, B., Shahbazi, M., Jauch, A., Engel, U., Patrizi, A., Sotillo, R., Bageritz, J., Alfonso, J., Bastians, H., Acebron, S. P. Abstract: The development and homeostasis of organisms rely on the correct replication, maintenance and segregation of their genetic blueprints. How these intracellular processes are monitored across generations of different human cellular lineages, and why the spatio-temporal distribution of mosaicism varies during development remain unknown. Here, we identify several lineage specification signals that regulate chromosome segregation fidelity in both human and mouse pluripotent stem cells. Through epistatic analyses, we find that that WNT, BMP and FGF form a signalling rheostat upstream of ATM that monitors replication fork velocity, origin firing and DNA damage during S-phase in pluripotency, which in turn controls spindle polymerisation dynamics and faithful chromosome segregation in the following mitosis. Cell signalling control of chromosome segregation fidelity declines together with ATM activity after pluripotency exit and specification into the three human germ layers, or further differentiation into meso- and endoderm lineages, but re-emerges during neuronal lineage specification. In particular, we reveal that a tug-of-war between FGF and WNT signalling in neural progenitor cells results in DNA damage and chromosome missegregation during cortical neurogenesis, which could provide a rationale for the high levels of mosaicism in the human brain. Our results highlight a moonlighting role of morphogens, patterning signals and growth factors in genome maintenance during pluripotency and lineage specification, which could have important implications for our understanding on how mutations and aneuploidy arise during human development and disease. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC
Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.04.21.537900v1?rss=1 Authors: Wen, B., Zheng, H.-X., Deng, D.-X., Zhang, Z.-D., Heng, J.-H., Liao, L.-D., Xu, L.-Y., Li, E.-M. Abstract: The translesion DNA synthesis (TLS) pathway mediated by proliferating cell nuclear antigen (PCNA) monoubiquitination is an essential mechanism by which cancer cells bypass DNA damage caused by DNA replication stress to maintain genomic stability and cell survival. Chromatin assembly factor 1 subunit A (CHAF1A) traditionally promotes histone assembly during DNA replication. Here, we revealed that CHAF1A is a novel regulator of the TLS pathway. High expression of CHAF1A is significantly associated with poor prognosis in cancer patients. CHAF1A promotes fork restart under DNA replication stress and maintains genome integrity. CHAF1A enhances the interaction between PCNA and E3 ubiquitin protein ligase RAD18 and promotes PCNA monoubiquitination, thereby promoting the recruitment of Y-family DNA polymerase Pol {eta} and enhancing cancer cell resistance to stimuli that trigger replication fork blockade. Mechanistically, CHAF1A-mediated PCNA monoubiquitination is independent of CHAF1A-PCNA interaction. CHAF1A interacts with both RAD18 and replication protein A2 (RPA2), mediating RAD18 binding on chromatin in response to DNA replication stress. Taken together, these findings improve our understanding of the mechanisms that regulate the TLS pathway and provide insights into the relationship between CHAF1A and the malignant progression of cancers. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC
Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.04.18.537310v1?rss=1 Authors: Stamatiou, K., Huguet, F., Spanos, C., Rappsilber, J., Vagnarelli, P. Abstract: Background: The proliferation antigen Ki-67 has been widely used in clinical settings for cancer staging for many years but investigations on its biological functions have lagged. Recently, Ki-67 was shown to regulate both the composition of the chromosome periphery and chromosome behaviour in mitosis as well as to play a role in heterochromatin organisation and gene transcription. However, a role for Ki-67 in regulating cell cycle progression has never been reported. The progress towards understanding Ki-67 function have been limited by the tools available to deplete the protein coupled to its abundance and fluctuation during the cell cycle. Results: Here we have used an auxin-inducible degron tag (AID) to achieve a rapid and homogeneous degradation of Ki-67 in HCT116 cells. This system, coupled with APEX2 proteomics and phospho-proteomics approaches, allowed us to show for the first time that Ki-67 plays a role during DNA replication. In its absence, DNA replication is severely delayed, the replication machinery is unloaded, causing DNA damage that is not sensed by the canonical pathways and dependant on HUWE1 ligase. This leads to replication and sister chromatids cohesion defects, but it also triggers an interferon response mediated by the cGAS/STING pathway in all the cell lines tested. Conclusions: We have unveiled a new function of Ki-67 in DNA replication and genome maintenance that is independent of its previously known role in mitosis and gene regulation. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC
On today's ID the Future, distinguished British physician and author David Galloway explains why he's convinced that the human fetal circulatory system is irreducibly complex and therefore beyond the reach of blind gradualistic evolution to have built. In his conversation with host and fellow physician Geoffrey Simmons, Galloway also mentions some molecular machines that he's convinced are irreducibly complex and shout intelligent design. The occasion for the conversation is Galloway's new book, Design Dissected. Source
Alfredo De Biasio, Assistant Professor, Bioscience, Biological and Environmental Science and Engineering Division, King Abdullah University of Science and Technology, SAUDI ARABIA speaks on "Human DNA replication under the microscope: Visualizing the lagging strand replisome at high-resolution using cryo-EM".
In this episode, we review the high-yield topic of DNA Replication from the Biochemistry section. Follow Medbullets on social media: Facebook: www.facebook.com/medbullets Instagram: www.instagram.com/medbulletsofficial Twitter: www.twitter.com/medbullets --- Send in a voice message: https://anchor.fm/medbulletsstep1/message
An IUPUI researcher is studying the role of DNA replication errors in cancer formation, and an IU Bloomington criminal justice professor is studying BIPOC progressive prosecutors and their efforts to reform criminal justice.
For life on Earth to grow, its genetic material must be copied and reproduced in a process known as DNA replication. Professor Michael O'Donnell, head of the Rockefeller University's DNA replication laboratory, has devoted his over 30-year career to the study of the protein complex that is responsible for just that – the replisome. Recently, Professor O'Donnell and his team uncovered exciting insights into the function of this remarkable piece of molecular machinery.
My AP Biology Thoughts Unit 6 Gene Expression and RegulationWelcome to My AP Biology Thoughts podcast, my name is Morgan and I am your host for episode # 106 called Unit 6 Gene Expression and Regulation: DNA Replication. Today we will be discussing the process by which cells replicate their DNA Segment 1: Introduction to DNA Replication Difference between prokaryotic and Eukaryotic DNA P is one circular piece of dna where eukaryotic are multiple linear chromosomes DNA replication is semi-conservative Double helix is split in two and then each new strand is synthesized so to new double helices are made, each with one old and one new strand very complex but very fast Extremely accurate (only 1 in a billion bases are messed up) Have to prime the DNA for replication Primers are short molecules that attach to the dna at the origin of replication Mde by the enzyme primase Helicase is the enzyme that unwinds the double helix- initiates the replication fork (where two strands split apart) Multiple replication forks in eukaryotic dna Topoisomerase checks problems in the DNA before replication and maintains the structure DNA polymerase is the enzyme that synthesizes the new DNA strand- reads the bases and matches up complementary nucleotides Segment 2: More About the process of replication Replication initiation can occur at both directions from the origin where the primer binds DNA polymerase can only add nucleotides in the 5 to 3 prime direction, and read the strand of dna in the 3 to 5 prime direction Leading strand is continuous Lagging strand is discontinuous, has to read and synthesize in short segments (okazaki fragments) Enzyme ligase seals together the fragments Energy needed for this process (remember forming bonds between the nucleotides requires energy) Segment 3: Connection to the Course Connection to mitosis S phase of mitosis is dna replication Necessary for cell division to make the same amount of chromosomes in daughter cells Process is close to the same for rna synthesis Leading and lagging strands Okazaki fragments and 3 to 5 prime direction vs 5 to 3 prime direction Thank you for listening to this episode of My AP Biology Thoughts. For more student-ran podcasts and digital content, make sure that you visit http://www.hvspn.com (www.hvspn.com). Music Credits: "Ice Flow" Kevin MacLeod (incompetech.com) Licensed under Creative Commons: By Attribution 4.0 License http://creativecommons.org/licenses/by/4.0/ Subscribe to our Podcast https://podcasts.apple.com/us/podcast/my-ap-biology-thoughts/id1549942575 (Apple Podcasts) https://open.spotify.com/show/1nH8Ft9c9f6dmo75V9imCk (Spotify) https://podcasts.google.com/search/my%20ap%20biology%20thoughts (Google Podcasts ) https://www.youtube.com/channel/UC07e_nBHLyc_nyvjF6z-DVg (YouTube) Connect with us on Social Media Twitterhttps://twitter.com/thehvspn ( @thehvspn)
Having worked with the likes of Freeman Dyson, we hear about the incredible achievements of Dr Bruce Alberts, winner of both the National medal of science in 2014 and the Lasker award in 2016. If you are interested in helping The Biotech Podcast please take 30 seconds to take the following survey: https://harry852843.typeform.com/to/caV6cMzGFull synopsis:00:00 - Intro01:30 - The scientific process09:51 - Scientific thinking and education24:25 - Writing 'Molecular biology of the cell', its intentions and its impacts41:32 - DNA replication - mechanisms, evolution and discovering the biochemistry1:03:54 - Book recommendations and advice1:08.09 - Freeman Dyson, Leroy Hood and the Human Genome project
This week we discuss DNA Replication.Find us on the internet!Our website - Teachmescience.co.ukEmail - teachmebiologycast@gmail.comTwitter - twitter.com/teachmebiocastInstagram - @teachmebiologycast
Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.11.11.378067v1?rss=1 Authors: Sato, K., Martin-Pintado, N., Post, H., Altelaar, M., Knipscheer, P. Abstract: G-quadruplex (or G4) structures are non-canonical DNA structures that form in guanine-rich sequences and threaten genome stability when not properly resolved. G4 unwinding occurs during S phase via an unknown mechanism. Using Xenopus egg extracts, we define a three-step G4 unwinding mechanism that is coupled to DNA replication. First, the replicative helicase (CMG) stalls at a leading strand G4 structure. Second, the DHX36 helicase mediates the bypass of the CMG past the intact G4 structure, which allows approach of the leading strand to the G4. Third, G4 structure unwinding by the FANCJ helicase enables the DNA polymerase to synthesize past the G4 motif. A G4 on the lagging strand template does not stall CMG, but still requires DNA replication for unwinding. DHX36 and FANCJ have partially redundant roles, conferring robustness to this pathway. Our data reveal a novel genome maintenance pathway that promotes faithful G4 replication thereby avoiding genome instability. Copy rights belong to original authors. Visit the link for more info
USELESS MODULE // I didn't think I'd actually get it to 45 seconds LOL
(Yes it has a different name). The 8-step process.
Melanie recAPs DNA Replication by reviewing the role of enzymes. DNA Replication is semiconservative and occurs during the S phase of the cell cycle in eukaryotic cells (1:20). How does the structure of DNA influence the process of replication? (1:40) The CED requires you to know the function of the following enzymes: topoisomerase (2:38), helicase (2:48), DNA polymerase (3:25), and ligase (4:35). There are distinctions between replication patterns in prokaryotes and eukaryotes (5:00).The Question of the Day asks (5:39) “What is the condensed, identical DNA strand called during mitosis?”Thank you for listening to The APsolute RecAP: Biology Edition!(AP is a registered trademark of the College Board and is not affiliated with The APsolute RecAP. Copyright 2020 - The APsolute RecAP, LLC. All rights reserved.)Website:www.theapsoluterecap.comEMAIL:TheAPsoluteRecAP@gmail.comFollow Us:INSTAGRAMTWITTER
This episode covers DNA replication and the cell cycle.
In this week's episode we look back at the 2nd week of the 2nd Semester and review the biggest concepts and activities over DNA Replication that were covered in class. In our 2nd segment I share some advice on ways to study and hints for the upcoming Ch. 11 and Ch. 16 Exam...Furthermore I announce a Study Session taking place to help those students who might want some extra help studying for the Upcoming Cell Communication and DNA Exam. In addition, in our new segment in the podcast called 5 Questions with Mr. V...I'll interview another special guest a hero, educator, and around great person Mr. Mora and ask him 5 questions so the audience gets to know him just a little bit better. Remember to subscribe, like, and please comment on the podcast on your podcast listening platform. You can also e-mail me at ovelas@neisd.net with any comments or feedback. You can also follow me on twitter at OscarVelasquez@APBiologyMrV. Students can always contact me and communicate with me via the Edmodo course website or APP. If you have questions you would like Mr. V to answer please e-mail me the questions or send them on Edmodo or Twitter. Also follow the new Instagram Page for the podcast "Evolving with Mr. V". I want to thank you for listening...I am your Host Mr. Oscar Velasquez "Master of the Biological Arts". Have a Great Week and May the Force be With You...I have Spoken. Big Shout Out to Free Music Achieve and SoundBible for the music and sound effects in the podcast.
This podcast covers DNA replication and central dogma. First, I breakdown DNA replication, discussing: conservative, semi-conservative, and dispersive replication, and the DNA replication mechanism. Then, I discuss transcription and translation, including: differences between prokaryotes and eukaryotes, mechanisms, and cellular location. Please email me if you have any comments or concerns: sasm6771@colorado.edu Thanks for listening!
Liz looks at DNA replication for your A Level Biology exam. In this episode, she will look at semi-conservative DNA replication, the enzymes involved in replication and the different models for DNA replication. Ideal for preparing for your A Level Biology exam. For more info visit https://www.senecalearning.com/blog/a-level-biology-revision/
Alex Wu is an American Cancer Society Postdoctoral Fellow in Johannes Walter's lab at Harvard Medical School, where he and his colleagues are focused on investigating the mechanisms of genome maintenance. In this conversation he goes deep into the science behind several of their recent publications, including a Nature paper in which they showed that TRAIP is a master regulator of DNA interstrand crosslink repair.
(Biochemistry) --- Support this podcast: https://anchor.fm/brad-richardson/support
(Biochemistry) --- Support this podcast: https://anchor.fm/brad-richardson/support
Chapter 12-2 DNA Replication by MrBiology360
Dr Costanzo talks to ecancertv at IFOM EMBL about vertebrate genome stability, focusing on the DNA replication and repair in vertebrate cells. Additionally he discusses his research using extracts derived from Xenopus laevis eggs, which allow extensive biochemical analysis which can be reproduced in vitro complex cell cycle events such as chromatin formation, nuclear assembly, semi-conservative DNA replication, chromosome assembly and mitotic spindle formation.
At the Intersection of DNA Replication and Genome Maintenance: from Mechanisms to Therapy
Iestyn Whitehouse, Memorial Sloan-Kettering CC, New York, speaks on "Coupling of gene enhancers and replication origins". This movie has been recorded by ICGEB Trieste at "At the Intersection of DNA Replication and Genome Maintenance: 2016 - from Mechanism to Therapy" conference.
At the Intersection of DNA Replication and Genome Maintenance: from Mechanisms to Therapy
Oscar Fernandez-Capetillo, Spanish National Cancer Res. Center, Madrid , speaks on "Mechanisms of resistance to anticancer therapies. "This movie has been recorded by ICGEB Trieste at "At the Intersection of DNA Replication and Genome Maintenance: 2016 - from Mechanism to Therapy" conference.
At the Intersection of DNA Replication and Genome Maintenance: from Mechanisms to Therapy
Sergei Mirkin, Tufts University, Medford, speaks on "Mechanisms of genome instability mediated by interstitial telomeric sequences". This movie has been recorded by ICGEB Trieste at "At the Intersection of DNA Replication and Genome Maintenance: 2016 - from Mechanism to Therapy" conference.
At the Intersection of DNA Replication and Genome Maintenance: from Mechanisms to Therapy
Wei Yang, NIDDK, NIH, Bethesda, speaks on "Molecular gymnastics during DNA translesion synthesis". This movie has been recorded by ICGEB Trieste at "At the Intersection of DNA Replication and Genome Maintenance: 2016 - from Mechanism to Therapy" conference.
At the Intersection of DNA Replication and Genome Maintenance: from Mechanisms to Therapy
Angelos Constantinou, Institute of Human Genetics, Montpellier, speaks on "A FANCM protein interaction screen reveals a pyrimidine catabolism enzyme required to prevent cell-intrinsic DNA replication stress ". This movie has been recorded by ICGEB Trieste at "At the Intersection of DNA Replication and Genome Maintenance: 2016 - from Mechanism to Therapy" conference.
At the Intersection of DNA Replication and Genome Maintenance: from Mechanisms to Therapy
James Berger, Johns Hopkins, Baltimore, speaks on "Structural mechanisms for initiating DNA replication". This movie has been recorded by ICGEB Trieste at "At the Intersection of DNA Replication and Genome Maintenance: 2016 - from Mechanism to Therapy" conference.
At the Intersection of DNA Replication and Genome Maintenance: from Mechanisms to Therapy
Philippe Pasero, Institute of Human Genetics, Montpellier, speaks on "SAMHD1 processes stalled forks and links DNA replication stress to inflammation". This movie has been recorded by ICGEB Trieste at "At the Intersection of DNA Replication and Genome Maintenance: 2016 - from Mechanism to Therapy" conference.
At the Intersection of DNA Replication and Genome Maintenance: from Mechanisms to Therapy
Puck Knipscheer, Hubrecht Institute, Utrecht, speaks on "How does the Fanconi pathway promote unhooking of DNA interstrand crosslinks?". This movie has been recorded by ICGEB Trieste at "At the Intersection of DNA Replication and Genome Maintenance: 2016 - from Mechanism to Therapy" conference.
At the Intersection of DNA Replication and Genome Maintenance: from Mechanisms to Therapy
David Cortez, Vanderbilt University, Nashville, speaks on "ETAA1 regulates ATR to maintain genome stability during DNA replication". This movie has been recorded by ICGEB Trieste at "At the Intersection of DNA Replication and Genome Maintenance: 2016 - from Mechanism to Therapy" conference.
At the Intersection of DNA Replication and Genome Maintenance: from Mechanisms to Therapy
Tony Carr, University of Sussex, Falmer, speaks on "Mechanisms of replication-associated genome rearrangement". This movie has been recorded by ICGEB Trieste at "At the Intersection of DNA Replication and Genome Maintenance: 2016 - from Mechanism to Therapy" conference.
At the Intersection of DNA Replication and Genome Maintenance: from Mechanisms to Therapy
Peter Burgers, Washington University, St.Louis, speaks on "The inner workings of the lagging strand maturation machinery". This movie has been recorded by ICGEB Trieste at "At the Intersection of DNA Replication and Genome Maintenance: 2016 - from Mechanism to Therapy" conference.
This week Rod & Mig discuss: Doctor Visits Chafing Making Babies Follow…
Professor Lander explains DNA Replication, the functions of the enzymes involved, and how problems that arise during replication are addressed.
DNA replication and Cancer The process of DNA replication is complex, and mistakes can lead to genome instability. Surveillance systems are not always successful which results in mutations that have the potential to inactivate genes or change their activity. This can lead to cancer, and many chemotherapeutic drugs are designed to disrupt DNA replication. A better understanding of these mechanisms can help us develop new drugs with reduced side effects.
DNA replication and Cancer The process of DNA replication is complex, and mistakes can lead to genome instability. Surveillance systems are not always successful which results in mutations that have the potential to inactivate genes or change their activity. This can lead to cancer, and many chemotherapeutic drugs are designed to disrupt DNA replication. A better understanding of these mechanisms can help us develop new drugs with reduced side effects.
In addition to mediating the transcriptional response to hypoxia, HIF-1α also inhibits proliferation under oxygen-limiting conditions.
J. F.X. Diffley Cancer Research UK, London Research Institute, Clare Hall Laboratories, South Mimms, UK speaks on "Investigating how DNA replication initiates in eukaryotes". This seminar has been recorded by ICGEB Trieste
Runtime 110:45 Memorial Sloan Kettering President and CEO Craig Thompson along with cancer biologist Andrea Ventura, molecular biologist Iestyn Whitehouse, and developmental biologist Jennifer Zallen explain how recent developments contribute to better treatments for cancer patients. read more
UNIT 11 - DNA Replication, Transcription, Translation
Genomes are composed of DNA, and a knowledge of the structure of DNA is essential to understand how it can function as hereditary material. DNA is remarkable, breathtakingly simple in its structure yet capable of directing all the living processes in a cell, the production of new cells and the development of a fertilized egg to an individual adult. DNA has three key properties: it is relatively stable; its structure suggests an obvious way in which the molecule can be duplicated, or replicated; and it carries a store of vital information that is used in the cell to produce proteins. The first two properties of DNA are analysed in this unit. This study unit is just one of many that can be found on LearningSpace, part of OpenLearn, a collection of open educational resources from The Open University. Published in ePub 2.0.1 format, some feature such as audio, video and linked PDF are not supported by all ePub readers.
Anindya Dutta, Biochemistry and Molecular Genetics, University of Virginia School of Medicine, Charlottesville, VA, USA speaks on "Ubiquitination pathways in the DNA replication and response to DNA damage". This seminar has been recorded by ICGEB Trieste
John Diffley, Chromosome Replication Laboratory, London Research Institute, Clare Hall Laboratories, South Mimms, London, UK speaks on "Mechanism and Regulation of DNA Replication in Yeast". This seminar has been recorded by ICGEB Trieste
How DNA molecules replicate themselves.
Transcript -- How DNA molecules replicate themselves.
Transcript -- How DNA molecules replicate themselves.
How DNA molecules replicate themselves.
DNA replication in mammalian cells occurs in discrete nuclear foci. Here we show that terminally differentiated myotubes can be induced to reenter S phase and show the same pattern of replication foci as cycling cells. We used this cellular system to analyze the interaction of cell cycle proteins with these foci in vivo. Cyclin A and cdk2, but not cyclin B1 and cdc2, were specifically localized at nuclear replication foci, just like the replication protein proliferating cell nuclear antigen. A potential target of cyclin A and cdk2 is the 34 kd subunit of replication protein A (RPA34). In contrast with the 70 kd subunit, which localizes to the foci, RPA34 was not detected at these replication sites, which may reflect a transient interaction. The specific localization of cyclin A and cdk2 at nuclear replication foci provides a direct link between cell cycle regulation and DNA replication.
Tissue-specific patterns of methylated deoxycytidine residues in the mammalian genome are preserved by postreplicative methylation of newly synthesized DNA. DNA methyltransferase (MTase) is here shown to associate with replication foci during S phase but to display a diffuse nucleoplasmic distribution in non-S phase cells. Analysis of DNA MTase-β-galactosidase fusion proteins has shown that association with replication foci is mediated by a novel targeting sequence located near the N-terminus of DNA MTase. This sequence has the properties expected of a targeting sequence in that it is not required for enzymatic activity, prevents proper targeting when deleted, and, when fused to β-galactosidase, causes the fusion protein to associate with replication foci in a cell cycle-dependent manner.
Sun, 1 Jan 1989 12:00:00 +0100 https://epub.ub.uni-muenchen.de/8666/1/8666.pdf Fritzenschaf, Hariolf; Becker, Karl F.; Conzelmann, Karl-Klaus; Helftenbein, Elke
Tue, 1 Jan 1980 12:00:00 +0100 https://epub.ub.uni-muenchen.de/5377/1/Zimmermann_Wolfgang_5377.pdf Weissbach, Arthur; Bolden, Arthur; Chen, Shih Min; Zimmermann, Wolfgang ddc:610, Medizin
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