DNA repair

damaged DNA seems to be an understudied subject, there is much to understand on the restoration of DNA damage, repair and DNA methylation. Genomic DNA can be modified by methylation but much of it is affected on a gene when silenced. When epigenetic modification has been implicated with cancer and aging it causes DNA methylation to also have an impact on the double strand of DNA analysis. Modification as such provoke deteriorating changes like aging found in multicellular organisms and DNA damage

Saccharomyces cerevisiae’s DNA repair system by disrupting its recombinational process post UV-irradiation Alexa Alana, Annie Cribb, Tommy Paranzino Biology 131- L8 ABSTRACT Saccharomyces cerevisiae was tested for the effects of ultraviolet (UV) irradiation in the presence of caffeine to observe whether the drug would enhance or inhibit the DNA’s recombinational repair process after the yeast has experienced UV damage. We hypothesized that caffeine would obstruct the yeast’s DNA repair process by interrupting

a dazzling display of choreography, proteins of the the DNA mismatch repair system (MMR) come together to fix replication errors, which results in an extraordinarily high degree of genomic fidelity.1-5 It is no wonder, then, that the MMR system has transcended almost all evolutionary stratification and is a highly conserved process across species. The MMR system is chiefly responsible for initiating cellular responses for several types of DNA lesions, including single-base mismatches and small insertion-deletion

cellular function, DNA repair mechanisms and cell cycle control. As a model organism, S. cerevisiae is one of the simplest eukaryote organism, having not only most major signaling pathways conserved, but also consisting of a genome of approximately 12.1 million base pairs in sixteen chromosomes. S. cerevisiaes, like other model organisms, have properties that make them suitable for biological studies: rapid growth, easy mutant isolation, a sequenced genetic system and a versatile DNA transformation system

Paul Modrich and the DNA Mismatch Repair System On December 10, 2015, three profound individuals received the Nobel Prize in chemistry for their work on DNA repair systems. Paul Modrich, Thomas Lindahl, and Aziz Sancar studied how the cell repairs and protects the information held in its DNA; specifically, Paul Modrich focused on DNA mismatch repair. Since DNA constantly replicates, damage and incorrect pairings are expected, but enzymes watch over DNA as it replicates and repair any errors that occur

almost like a pause. It gives the body time to repair the dna cells or dispose of the ones that cannot be fixed. Once it is fixed then the P53 releases the repaired cell and continues on to the next phase. The G1 phase in a 150 minute cell cycle would be around 30 minutes. However in the mutated cancer cell the p53 stops working and so the damaged cells are never repaired or killed off and continue with the phases. During the S phase in a normal cell basic dna synthesis occurs as well as chromosome

BRCA 2 INFORMATION BRCA1 and BRCA2 share a lot of similarities. BRCA2 is also a cause for hereditary breast cancer and is also responsible for tumor suppressor proteins. BRCA2 is located on chromosome thirteen. BRCA2 can repair breaks within DNA, such as DSBs and can regulate cytokinesis. Cytokinesis is a process during cell division where the cytoplasm, the fluid inside the cells that is enclosed by the cell membrane, of one parent cells splits into two daughter cells. BRCA2 mutations are more commonly

1. What are the different restriction points of the cell cycle? Describe each. G1 (Restriction) Checkpoint * End of G1, just before onset of the S phase (DNA replication) * Yeast “start”; other eukaryotes “restriction point” * The options for the cell at this point: * divide, delay division, or exit the cell cycle * Cells can exit the cell cycle at this point into an arrested stage (G0) * When this checkpoint is passed, cdk4 and cyclin D

that Progeria is caused by a single base mutation in LMNA which results in the production of a mutant Lamin A protein product called Progerin. (Blondel and others 2014) Progerin is toxic and causes distribution of the nuclear structure, defects in DNA repair processes and other issues that are associated with the premature aging that their bodies

Introduction: A New York Times op-ed article on May 14, 2013 revealed that Angelina Jolie underwent a double mastectomy (Jolie). She did not have cancer. What would prompt a healthy individual to perform such drastic and disfiguring surgery if her life were not in danger? It turns out that she carries a breast cancer gene mutation, BRCA1, which increases the chances of developing breast and ovarian cancer. The availability of genetic testing has caused prophylactic double mastectomy rates to increase